Sleep is usually a big issue for people with autoimmune disorders. Based on a poll by the Autoimmune Association, 98% of people with autoimmune diseases suffer from fatigue. In fact, sleep is one of the main pillars of healing that I discuss with all of my clients. There’s a strong connection between sleep and inflammation. Today we are talking all about sleep and ways you can use sleep to improve your autoimmune disease.
Sleep and Inflammation
Sleep plays a major role in inflammation and autoimmune disease activity. Most people who suffer from flares find that sleep can be a major issue. Additionally, lack of sleep and/or sleep deprivation can actually trigger some autoimmune diseases.
When we live with an autoimmune disease, our biggest goal to improve our quality of life is to reduce or eliminate flares. Flares are usually caused by underlying, chronic inflammation. When inflammation is present, it affects the sleep center in your brain, located in your hypothalamus.
Inflammation can also alter your sleep cycles. Your sleep cycles are an important part of getting restful and regenerative sleep. Each part of the sleep cycle is equally important. Chronic inflammation causes the body to spend less time in both REM sleep and deep sleep. These 2 sleep cycles have important functions to help your body rest and recover:
Deep Sleep: Deep sleep is the point in the sleep cycle where your body starts to repair and grow. The brain flushes out waste products during this phase of sleep.
REM Sleep: This phase of sleep is important for memory, learning, and problem-solving. It is also when your body releases endorphins for pain relief and growth hormones.
How to get better sleep?
Sleep is something that most people, unfortunately, take for granted or don’t prioritize. When you live with an autoimmune disease, sleep is incredibly critical. We also need more sleep than the average person – 7 hours just isn’t going to cut it. Getting better sleep is a process and it doesn’t happen overnight. Here are some tips to improve your quality of sleep:
1) Establish a sleep routine
Sleep routines signal your body that sleep is coming. It helps you wind down and prepare yourself and your hormones for sleep. Doing a few (and I mean 1-2 things) repetitive activities every night before bedtime can really help you fall asleep faster and get better quality sleep. These activities do not have to be super complicated either. They might include:
Wearing blue light-blocking glasses 1-2 hours before bedtime to preserve your melatonin production to help you fall asleep faster.
Write out a to-do list before going to sleep so you don’t have racing thoughts about what you need to accomplish tomorrow.
Place all electronics on airplane mode or remove them from your bedroom before going to bed.
Stop doing work 1-2 hours before bedtime to allow your mind to rest and calm down
Do a sleep meditation
2) Get on a regular sleep schedule daily
Going to bed and waking up within the same 1-hour window every day (yes, including weekends) helps stabilize your circadian rhythm. Having a synchronized circadian rhythm helps regulate hormones, it gets your body in sync with the light and dark cycle of the Earth and establishes a master clock with which all of your organ systems also connect, making your body work a little more efficiently.
When your circadian rhythm is not synchronized or erratic, it can have a number of consequences, including:
Throws off your melatonin and cortisol curves making it hard for you to fall asleep and wake up.
Affects your hormones and metabolism, making it harder for you to lose weight.
May increase inflammation
Affects your immune system.
One easy way to stabilize your circadian rhythm is by having a consistent sleep schedule. The other easy thing you can do is after you wake up, get outside as soon as possible (ideally before 10 am) and get direct sunlight on your eyes. This signals to your body that it’s time to be awake and get your day started.
As you can see, sleep and good quality sleep can really help you feel better when you have an autoimmune disease. If you try any of my tips and find that it helps, please contact me and let me know! Additionally, for more information on the connection between autoimmune diseases, follow me on Instagram, Facebook, and YouTube.
Autoimmune diseases are a large collection of conditions where cells in the body begin to attack the body’s own tissues. Autoimmune diseases can affect almost every part of the body. The eyes are no exception. In fact, the eyes are very commonly affected in many autoimmune diseases.
Here, we’ll review some of the conditions that can arise when autoimmune diseases target the eyes. We’ll also look at the symptoms of these conditions and common treatments. Finally, we’ll discuss some of the medicines used to control autoimmune diseases that can have side effects on the eyes.
Which autoimmune diseases have symptoms that affect the eyes?
Some autoimmune diseases that commonly affect the vision and eyes are:
Rheumatoid arthritis
Thyroid diseases
Multiple sclerosis (MS)
Other autoimmune conditions that can cause problems with vision and the eyes are:
Sjogren’s syndrome
Lupus
Inflammatory bowel disease (Crohn’s and ulcerative colitis)
Ankylosing spondylitis
Eye problems can also be a feature of some rarer autoimmune conditions, such as:
Polyarteritis nodosa
Granulomatosis with polyangiitis (also known as Wegener’s)
Scleroderma
Behcet’s disease
Reactive arthritis
What are the different eye problems that can be caused by autoimmune diseases?
Dry eyes
Dry eyes is caused by not having enough tears on the surface of your eyes. Dry eyes can cause gritty, irritated eyes and blurry vision. When severe, dry eyes can cause permanent damage to your cornea and affect your vision.
Dry eyes is the main symptom in Sjogren’s syndrome. Dry eyes in Sjogren’s syndrome and other autoimmune diseases is caused by inflammation of the lacrimal gland, the gland that makes liquid tears.
When dry eyes occurs with other autoimmune diseases — like rheumatoid arthritis, systemic lupus erythematosus (SLE), and scleroderma — it is sometimes called secondary Sjogren’s syndrome.
Over-the-counter artificial tears, lubricating gels, and ointments can all help with dry eyes caused by autoimmune diseases. These work by adding moisture back to the eyes’ surface. Prescription eye drops such as steroids, cyclosporine (Restasis), and lifitegrast (Xiidra) may also help dry eyes. Serum tears are another effective way to treat dry eyes. Punctal plugs can be used to close the tear drainage system and keep natural and artificial tears on the eye’s surface longer.
Scleritis
Scleritis is when the white part of the eye becomes inflamed. It causes redness in the white part, and it also often causes deep, aching pain in the eyes. If left untreated, scleritis can cause thinning of the sclera to the point where it may open up, or perforate. This can cause permanent damage to the eye and your vision.
Rheumatoid arthritis is one of the more common autoimmune diseases associated with scleritis.
Other autoimmune diseases that can cause scleritis include:
Lupus
Inflammatory bowel disease
Sjogren’s syndrome
Scleroderma
Polyangiitis (formerly Wegener’s)
Scleritis is typically treated with oral non-steroidal anti-inflammatory medications (NSAIDs) or steroids to control the inflammation. Steroid drops such as prednisolone acetate (Pred Forte, Omnipred) or NSAID drops such as ketorolac (Acular, Acular LS, Sprix) may also be used.
Uveitis
Uveitis is when the inside of the eye, also called the uvea, becomes inflamed. There are three main types of uveitis: anterior, intermediate, and posterior.
Anterior uveitis
Also called iritis, anterior uveitis occurs in the front of the eye. It causes redness, painful light sensitivity, and blurred vision. If it is not controlled, anterior uveitis can cause scar tissue to form inside the eye and permanently damage the vision.
Anterior uveitis can occur in people with ankylosing spondylitis and inflammatory bowel disease. Sarcoidosis also causes anterior uveitis.
Painless anterior uveitis can occur in children with rheumatoid arthritis (a condition called juvenile idiopathic arthritis, or JIA). This is why children with JIA need regular eye exams.
Anterior uveitis is usually treated first with steroid eye drops like prednisolone acetate or difluprednate (Durezol). If these drops do not help, steroid injections around the eye and/or steroids by mouth may be prescribed. As with autoimmune diseases, if the condition is not controlled with steroids or requires frequent or long-term steroids, then steroid-sparing medicines may be recommended and prescribed.
Intermediate uveitis
Intermediate uveitis occurs in the center of your eye, in the vitreous cavity. Intermediate uveitis can cause blurry vision and floaters in your vision. Unlike anterior uveitis, it does not typically cause pain.
People who have multiple sclerosis (MS) are known to develop intermediate uveitis, which is also sometimes called pars planitis. It is not yet known if MS directly causes intermediate uveitis or if people with MS are simply more prone to developing this condition.
Like anterior uveitis, intermediate uveitis is treated with steroids.
Posterior uveitis
Posterior uveitis occurs in the retina or choroid, which is in the back part of the eye.
With this condition, the retina and/or the blood vessels that supply the retina become inflamed. This causes blurry vision, and it is usually not painful.
Posterior uveitis can be a symptom of sarcoidosis, lupus, and a rare condition called Vogt-Koyanagi-Harada (VKH) syndrome.
Posterior uveitis is typically treated with steroids injected in or around the eye, as well as steroid medication by mouth.
Panuveitis
Very rarely, all parts of the eye can become inflamed. This is called panuveitis. Panuveitis is treated with steroid medication by mouth.
Optic neuritis
Optic neuritis is swelling of the optic nerve. The optic nerve is the nerve in the back of the eye, and it’s the main connection between the eye and the brain. When it becomes inflamed, it is called optic neuritis. Optic neuritis causes blurry vision, loss of peripheral vision, and pain with eye movements.
Optic neuritis can happen to people without autoimmune disease. But it also happens to be very strongly linked to MS. In fact, optic neuritis is one of the common early signs of MS. Between 15% and 20% of people have optic neuritis as a first symptom of MS, and as many as 50% of people with MS have had optic neuritis in the previous 15 years.
Optic neuritis can also happen along with uveitis in other autoimmune diseases, such as lupus.
Optic neuritis may get better without treatment. But prescription steroid medication taken either by mouth or intravenously (IV) will usually help it heal more quickly.
Thyroid Eye Disease
Thyroid Eye Disease (TED) — also called Graves’ Eye Disease — occurs when the cells that attack the thyroid gland also attack parts around the eye. This condition causes the muscles around the eye to swell, the eyelids to tighten, and the eyeballs to bulge. This can make it more difficult for the eyelids to close. The swollen eye muscles can also put pressure on the optic nerve. These changes can cause blurred vision and double vision.
Common treatments for TED include over-the-counter lubricants for dry eyes and steroid medicine by mouth or IV to calm the inflammation. More recently, monoclonal antibodies like Tepezza have been used for TED. When TED changes the eye muscles and eyelids, corrective surgery can be an option.
Can autoimmune diseases lead to blindness if left untreated?
Most autoimmune diseases can be managed with medication. But serious damage and even blindness can happen with autoimmune diseases if they are not treated. Your eye doctor (ophthalmologist) and your autoimmune specialist (rheumatologist) will work together to help treat the problems in the eyes that arise with autoimmune diseases.
Can medications like hydroxychloroquine that treat autoimmune diseases cause eye damage?
Hydroxychloroquine is a medication used to treat many autoimmune diseases. It can be very effective, with few side effects. Rarely, hydroxychloroquine can cause damage to the cells in the macula — the center of the retina — and hurt your vision. This problem, called hydroxychloroquine maculopathy, is more likely if you’re taking higher doses for 5 years or more. If you’re taking hydroxychloroquine, you should have regular eye exams to watch for early signs of hydroxychloroquine maculopathy.
Steroids are often prescribed to control autoimmune diseases. Steroids work very well in most cases and rarely cause serious side effects if used short term. However, they have many side effects if used long term. Steroids can cause problems with the eyes like cataracts and glaucoma.
What over-the-counter medicines can help treat eye symptoms of autoimmune diseases?
Over-the-counter artificial tears, lubricating gels, and ointments can all help with dry eyes caused by autoimmune disease. These work by adding moisture back to the eyes’ surface. Inflammatory conditions are sometimes treated with oral NSAIDs that are available over the counter.
The bottom line
Autoimmune diseases can have many effects on your body, including your eyes. Changes in your vision and your eyes can occur when autoimmune diseases are uncontrolled. It’s important to monitor your eyes and your vision when taking some medications used to control autoimmune diseases. An eye doctor can work with your primary and autoimmune doctor to help diagnose and treat problems in the eye due to autoimmune diseases.
Autoimmune sleep disorders occur when the immune system turns on the brain’s own sleep-regulating machinery, destroying neurons and disrupting the circuits that control wakefulness, dreaming, and consciousness itself. The damage can be catastrophic, up to 95% of critical wake-promoting neurons gone, yet patients often spend a decade being told they’re depressed or lazy before anyone orders the right test. Understanding what’s actually happening changes everything about how these conditions are diagnosed and treated.
Key Takeaways
In narcolepsy type 1, the immune system destroys hypocretin-producing neurons in the hypothalamus, eliminating the brain’s primary wake-promoting signal
Specific HLA genetic variants significantly raise the risk of autoimmune sleep disorders, though genes alone don’t determine who develops them
Viral infections, including the 2009 H1N1 pandemic, have been linked to triggering autoimmune sleep disorders in genetically susceptible people
Autoimmune encephalitis can produce a wide range of sleep disturbances, insomnia, hypersomnia, disrupted sleep-wake cycles, depending on which brain region the antibodies target
Treatment typically combines immunotherapy to address the underlying attack with symptom management and lifestyle changes
What Are Autoimmune Sleep Disorders?
Sleep isn’t just rest. It’s an active, precisely orchestrated neurological process controlled by specific brain circuits, and like any biological system, those circuits can become targets for a misdirected immune response.
Autoimmune sleep disorders are conditions in which the immune system attacks components of the brain’s sleep-wake regulatory system. The targets vary: in some conditions, it’s the neurons that produce wake-promoting chemicals; in others, it’s specific cell-surface receptors or synaptic proteins. What they share is a common logic, the immune system mistakes “self” for “enemy” and fires accordingly.
These disorders sit at a strange intersection of neurology and immunology, which partly explains why they’re so frequently missed.
When someone can’t sleep, the first instinct is rarely to check their antibody levels. Disrupted sleep patterns have many causes, and the autoimmune ones tend to hide behind more familiar explanations, depression, laziness, poor sleep habits, for years.
Estimates suggest that up to 20% of people with autoimmune diseases experience significant sleep-related problems, though the true figure is likely higher given how often these conditions go unrecognized. The downstream consequences reach well beyond tired mornings: cognitive impairment, mood disruption, metabolic dysregulation, and reduced quality of life compound over time.
What Autoimmune Diseases Cause Sleep Problems?
Some autoimmune conditions attack the sleep system directly.
Others disrupt sleep indirectly through inflammation, pain, or the effects of treatment.
Lupus, for instance, is associated with sleep disturbances through several overlapping mechanisms, how lupus affects sleep involves inflammatory cytokines crossing into the central nervous system, pain flares interrupting sleep architecture, and fatigue that paradoxically coexists with poor-quality rest. Rheumatoid arthritis and multiple sclerosis follow similar patterns.
Hashimoto’s thyroiditis, an autoimmune thyroid condition, is increasingly linked to Hashimoto’s disease and sleep apnea, where thyroid dysfunction alters upper airway muscle tone and respiration during sleep.
Even the medications used to treat autoimmune conditions can be culprits, corticosteroids, for example, have well-documented effects on how corticosteroids affect sleep quality, often suppressing slow-wave sleep and increasing nighttime arousal.
Then there are the conditions where the sleep system itself is the primary target, narcolepsy, autoimmune encephalitis, and related disorders, where the immune attack is not collateral damage but the central event.
Is Narcolepsy an Autoimmune Disorder?
The evidence is now strong enough that most sleep medicine specialists treat narcolepsy type 1 as an autoimmune disease, even though the precise autoantibody responsible hasn’t been definitively confirmed in all cases.
Here’s what we know. Narcolepsy type 1 is defined by the near-total loss of hypocretin (also called orexin), a neuropeptide produced by a small cluster of neurons in the hypothalamus that acts as the brain’s primary “stay awake” signal. Post-mortem brain tissue from people with narcolepsy shows a dramatic reduction in these neurons, with some studies finding losses of 85–95% compared to controls.
That’s not a gradual decline. That’s destruction.
The genetic fingerprint supports an autoimmune mechanism. More than 98% of people with narcolepsy-cataplexy carry the HLA-DQB1*06:02 allele, a gene variant that influences how the immune system recognizes self from non-self. HLA genes are the hallmark of autoimmune susceptibility; their strong association with narcolepsy is one of the clearest genetic signals in all of sleep medicine.
Complex interactions involving HLA-DR and HLA-DQ alleles confer risk across multiple ethnic populations, suggesting the mechanism is not population-specific.
The environmental trigger picture strengthened considerably after 2009. Following the H1N1 influenza pandemic, Finland and several other countries recorded sharp increases in childhood narcolepsy cases. In Finland specifically, the spike followed both natural H1N1 infection and the Pandemrix vaccine used in the pandemic response, pointing to molecular mimicry, where a pathogen or vaccine antigen resembles a self-protein closely enough to provoke an immune response that then turns on the brain.
In narcolepsy type 1, the immune system can destroy up to 95% of the roughly 70,000 neurons responsible for maintaining wakefulness, yet the average time from symptom onset to diagnosis is still around 10 years. The biological devastation is nearly complete before most patients ever hear the word “hypocretin.”
Common Autoimmune Sleep Disorders
Narcolepsy type 1 is the most studied, but it’s not the only condition in this category.
Narcolepsy Type 1 produces a recognizable cluster: overwhelming daytime sleepiness, cataplexy (sudden muscle weakness triggered by emotion, laughing, surprise, anger), sleep paralysis, and hypnagogic hallucinations at sleep onset.
The cataplexy is the telling symptom, it’s essentially REM sleep intrusion into wakefulness, the body briefly losing muscle tone the way it would during dreaming.
Narcolepsy Type 2 shares the sleepiness without confirmed cataplexy. Hypocretin levels may be normal or borderline. Whether it’s a distinct condition or an early or incomplete form of type 1 is still debated.
Idiopathic Hypersomnia involves profound daytime sleepiness despite sleeping 10–12 hours or more.
Sleep is long but unrefreshing, people wake feeling worse than when they went to bed, a pattern known as non-restorative sleep. An autoimmune mechanism is suspected in some cases; there’s evidence of a GABA-A receptor-potentiating substance in the cerebrospinal fluid of some patients, though the field is still working out the details.
Kleine-Levin Syndrome is rare and strange. Affected people, predominantly adolescent males, cycle in and out of episodes lasting days to weeks where they sleep up to 20 hours a day, eat compulsively, experience cognitive confusion, and show altered behavior.
Between episodes, they’re completely normal. The episodic, relapsing-remitting pattern and the presence of HLA associations in some patients suggest immune involvement, though direct autoantibody evidence remains limited.
Autoimmune encephalitis encompasses a growing list of antibody-mediated brain disorders, many of which produce dramatic sleep disturbances as part of their presentation, covered in more detail below.
Comparison of Major Autoimmune Sleep Disorders Disorder Autoimmune Target / Mechanism Core Sleep Symptoms Key Diagnostic Test First-Line Treatment Narcolepsy Type 1 Destruction of hypocretin neurons (hypothalamus) Excessive daytime sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations MSLT + CSF hypocretin level Sodium oxybate, modafinil, antidepressants for cataplexy Narcolepsy Type 2 Unknown; no confirmed hypocretin loss Excessive daytime sleepiness (no cataplexy) MSLT Modafinil, stimulants Idiopathic Hypersomnia Suspected GABA-A receptor potentiation Long, unrefreshing sleep; severe sleep inertia MSLT + sleep diary/actigraphy Modafinil, clarithromycin (off-label), flumazenil Kleine-Levin Syndrome Unknown; HLA associations suspected Recurrent hypersomnia episodes (up to 20 hrs/day), hyperphagia, cognitive changes Clinical criteria + EEG/MRI Lithium (prophylaxis), supportive care Autoimmune Encephalitis Neuronal surface or synaptic antibodies Insomnia, hypersomnia, or disrupted sleep-wake cycle depending on antibody Antibody panel (serum + CSF) IVIG, plasma exchange, corticosteroids, rituximab
Can Autoimmune Encephalitis Cause Insomnia and Sleep Disturbances?
Yes, and the sleep symptoms can be severe enough to be the presenting complaint before anyone thinks to look for an encephalitis diagnosis.
Autoimmune brain diseases caused by antibodies attacking neuronal proteins produce some of the most dramatic sleep phenotypes in medicine. Anti-NMDA receptor encephalitis, the most common form, can cause complete sleep-wake cycle reversal, patients awake at night, unresponsive during the day, along with psychosis, seizures, and movement abnormalities.
The sleep disruption here isn’t secondary to the brain inflammation; it’s a direct consequence of NMDA receptors being blocked at key regulatory sites.
Anti-IgLON5 disease is a more recently described condition that’s particularly striking from a sleep perspective. Patients develop an unusual parasomnia, abnormal, complex behaviors during sleep that don’t fit neatly into any standard category, alongside breathing problems during sleep, gait disturbances, and cognitive decline. Brain tissue from affected patients shows tau accumulation in sleep-regulating regions of the brainstem, suggesting the autoimmune attack triggers a secondary neurodegeneration.
Morvan’s syndrome, caused by CASPR2 or LGI1 antibodies, produces severe insomnia, sometimes total insomnia, along with neuromyotonia (muscle twitching), hallucinations, and dysautonomia.
The insomnia in Morvan’s can be so profound it resembles fatal familial insomnia, a prion disease. Recognition matters here, because unlike the prion disease, Morvan’s can respond to immunotherapy.
Autoimmune Encephalitis Antibodies and Their Sleep-Related Manifestations Antibody Target Associated Condition Sleep Disturbance Produced Response to Immunotherapy NMDA receptor Anti-NMDA receptor encephalitis Sleep-wake cycle reversal, hypersomnia Generally good with early treatment LGI1 LGI1 antibody encephalitis Insomnia, REM sleep behavior disorder, faciobrachial dystonic seizures Moderate to good CASPR2 Morvan’s syndrome, CASPR2 encephalitis Severe or total insomnia, abnormal movements in sleep Variable; some cases respond well IgLON5 Anti-IgLON5 disease Complex parasomnia, sleep-disordered breathing, NREM and REM abnormalities Partial; neurodegeneration limits recovery GABA-B receptor GABA-B encephalitis Insomnia, status epilepticus Moderate response AMPA receptor AMPA receptor encephalitis Sleep dysregulation, psychiatric symptoms Variable
Are There Sleep Disorders Caused by Antibodies Attacking the Brain?
This is exactly the right question, and the answer has been reshaping neurology over the past two decades.
The discovery of specific neuronal surface antibodies has transformed conditions once written off as “psychiatric” or “unknown encephalopathy” into diagnosable, treatable autoimmune diseases.
The key insight is that antibodies targeting surface proteins on neurons, receptors, ion channel complex proteins, can alter neuronal function in real time, often reversibly, in contrast to antibodies that target intracellular proteins (which typically cause damage through T-cell mechanisms and are less reversible).
Sleep is particularly vulnerable because the circuits controlling it are concentrated in specific brainstem and hypothalamic structures. When antibodies hit the wrong receptor in the wrong place, the whole system can go haywire: the switch between wakefulness and sleep stops working reliably, REM intrudes into wakefulness, or the person simply cannot maintain sleep at all.
The expanding list of pathogenic antibodies, including those targeting NMDA, LGI1, CASPR2, GABA-B, AMPA, and IgLON5, means that what was once an idiopathic sleep problem may turn out, on the right antibody panel, to be a treatable autoimmune condition.
Testing is still underutilized, partly because the conditions are rare and partly because sleep complaints rarely trigger an autoimmune workup in routine practice.
Causes and Mechanisms: How Does the Immune System Disrupt Sleep?
The relationship between the immune system and sleep runs deeper than most people realize. Sleep itself is immunomodulatory, it’s when the body consolidates immune memory, reduces inflammatory load, and resets cytokine levels. Chronic sleep restriction, even modest reductions to 6 hours a night, measurably elevates inflammatory markers including IL-6 and TNF-alpha.
The immune system and sleep are not separate systems with occasional interactions; they’re deeply co-regulated.
In autoimmune sleep disorders, this relationship breaks down in a specific direction: instead of sleep supporting immune balance, the immune system actively attacks the architecture of sleep. Three broad mechanisms drive this.
Molecular mimicry is the best-supported trigger for narcolepsy. A viral protein, or occasionally a vaccine antigen, resembles a self-peptide closely enough that the immune response generated against the pathogen cross-reacts with brain tissue.
The H1N1 connection is the clearest example: a surface protein on the virus shares structural similarities with a hypocretin receptor peptide, and in genetically susceptible people, the immune response overshoots.
Direct antibody-mediated damage drives the encephalitis syndromes. Here, antibodies bind to neuronal surface proteins, blocking their function, triggering receptor internalization, or activating complement to directly destroy synapses.
Neuroinflammation, diffuse inflammation within the central nervous system, can disrupt sleep-wake regulation without a specific autoantibody target. Elevated cytokines in the brain shift sleep architecture toward lighter, more fragmented sleep, suppress slow-wave sleep, and can alter circadian timing.
Understanding how stress and anxiety trigger autoimmune responses adds another layer. Chronic psychological stress dysregulates the HPA axis and immune signaling in ways that can lower the threshold for autoimmune activation in susceptible individuals.
Genetic Risk Factors for Autoimmune Sleep Disorders
Genetics in this field centers heavily on the HLA system, a set of genes on chromosome 6 that encodes proteins used by the immune system to distinguish self from non-self. These genes vary enormously between individuals, and certain variants load the dice for specific autoimmune conditions.
In narcolepsy type 1, the HLA association is one of the strongest seen in any complex disease. The HLA-DQB1*06:02 allele is present in over 98% of narcolepsy-cataplexy patients across multiple ethnic groups — European, Japanese, African-American populations — suggesting a universal mechanism rather than a population-specific quirk.
Carrying the allele doesn’t guarantee narcolepsy; the population prevalence of the allele is roughly 25% in Europeans, while narcolepsy affects only about 1 in 2,000 people. But its near-universal presence in affected individuals points squarely at the immune system as the mediating mechanism.
HLA Genetic Risk Factors Associated With Autoimmune Sleep Disorders Disorder Associated HLA Allele Estimated Relative Risk Populations with Confirmed Association Narcolepsy Type 1 HLA-DQB106:02 >200-fold vs. non-carriers European, Japanese, African-American Narcolepsy Type 1 HLA-DQA101:02 High (in linkage with DQB106:02) European, Japanese Kleine-Levin Syndrome HLA-DQB102 Modest (data limited) European Anti-IgLON5 disease HLA-DRB110:01, HLA-DQB105:01 Elevated (small cohort data) European Autoimmune Encephalitis (general) Variable by antibody type Moderate Mixed populations
What Are the Symptoms of Autoimmune Sleep Disorders?
The symptom picture shifts depending on which part of the sleep system is targeted, but several patterns appear consistently across conditions.
Excessive daytime sleepiness is the most common presenting complaint, not ordinary tiredness but an overwhelming, irresistible pressure to sleep that strikes at inappropriate times. Eating, driving, mid-conversation.
Patients often describe it as a physical force rather than a preference.
Cataplexy, when present, is diagnostic in character: sudden, emotion-triggered muscle weakness ranging from a jaw drop or knee buckle to a complete collapse, while the person remains conscious throughout. It’s one of the most bizarre and underdiagnosed symptoms in medicine.
Sleep paralysis and hypnagogic hallucinations, the inability to move at sleep onset or awakening, often accompanied by vivid, realistic visions or sensations, are experienced by many people without narcolepsy, but in narcolepsy they’re more frequent and more distressing.
Cognitive symptoms are common and often the most disabling in daily life. The autoimmune-related brain fog that accompanies these conditions goes beyond sleepiness; it involves genuine deficits in processing speed, working memory, and word-finding that don’t fully resolve with stimulant treatment.
Autoimmune encephalitis adds psychiatric symptoms, paranoia, hallucinations, personality change, to the mix, and these often dominate the early clinical picture before the sleep disturbance becomes apparent. Understanding the connection between autoimmune disease and mental illness matters here, because patients presenting to psychiatry with new-onset psychosis in their 20s or 30s may have an encephalitis diagnosis missed for months.
Night sweats and thermoregulatory disturbances are worth noting too.
Night sweats during illness have immunological roots, and in autoimmune conditions involving hypothalamic dysfunction, temperature dysregulation during sleep is not unusual.
How Do Doctors Diagnose Autoimmune-Related Sleep Disorders?
Diagnosis is often a long, frustrating process, partly because these conditions are rare, partly because the symptoms overlap substantially with more common disorders, and partly because the right tests aren’t always ordered.
The core diagnostic workup for narcolepsy combines two studies. Polysomnography (an overnight sleep study) establishes baseline sleep architecture and rules out other disorders, particularly sleep apnea, which causes daytime sleepiness through a completely different mechanism.
The multiple sleep latency test (MSLT), conducted the following day, measures how quickly a person falls asleep across five 20-minute nap opportunities. Falling asleep in under 8 minutes on average, with REM sleep appearing in two or more naps, is the electrophysiological signature of narcolepsy.
CSF hypocretin measurement is the definitive test when narcolepsy type 1 is suspected: levels below 110 pg/mL are diagnostic. HLA typing adds supporting evidence but can’t confirm or exclude the diagnosis on its own given how common the risk alleles are in the general population.
For autoimmune encephalitis, antibody panels in both serum and cerebrospinal fluid are essential, serum alone misses a meaningful proportion of cases.
MRI may show signal changes in limbic regions, though it’s often normal early in the disease. EEG frequently shows diffuse slowing or, in limbic encephalitis, characteristic patterns.
Accurate diagnosis depends on recognizing how each condition presents. Mapping each sleep disorder to its defining symptoms is the first step, and the one most often skipped when clinicians default to common explanations for daytime sleepiness.
The differential is substantial. Chronic sleep deprivation mimics hypersomnolence. Depression causes fatigue and disrupted sleep. Obstructive sleep apnea causes exactly the same pattern of morning fog and afternoon crashes as narcolepsy. The distinguishing features matter, and getting them wrong delays treatment by years.
Treatment Options for Autoimmune Sleep Disorders
Treatment has two parallel goals: suppress the immune attack, and manage the symptoms it’s caused. These are not always the same problem.
Immunotherapy is the most logical intervention when an active autoimmune process is identified. For autoimmune encephalitis, intravenous immunoglobulin (IVIG) and plasma exchange are first-line acute treatments.
Corticosteroids follow. For refractory cases, rituximab (which depletes B cells) or cyclophosphamide may be used. The earlier immunotherapy is started, the better the outcomes, delay allows more neuronal damage to accumulate, some of which may be irreversible.
For narcolepsy type 1, the timing problem is fundamental: by the time symptoms appear and a diagnosis is made, most of the hypocretin neurons are already gone. Immunotherapy at that stage has shown limited benefit in most cases, though there’s ongoing research into whether early intervention in newly diagnosed patients, within weeks of onset, might preserve some neurons.
Symptomatic treatment remains the mainstay for established narcolepsy. Sodium oxybate (GHB) taken at night consolidates nighttime sleep and substantially reduces cataplexy and daytime sleepiness, it’s the most effective pharmacological option currently available.
Wake-promoting agents (modafinil, armodafinil) and stimulants (methylphenidate, amphetamines) address daytime sleepiness. Antidepressants at low doses suppress REM sleep and reduce cataplexy.
A newer agent, pitolisant, acts on histamine receptors to promote wakefulness without the scheduling restrictions of controlled substances. Low-sodium oxybate formulations (Lumryz, Xywav) have improved tolerability for some patients.
Various sleep aids for autoimmune conditions can help with symptom management under medical supervision, though they work best as part of a broader treatment plan rather than as standalone solutions.
Lifestyle adaptations matter more than they’re usually given credit for.
Scheduled naps, two brief naps timed strategically across the day, can reduce total stimulant requirements and improve functioning in narcolepsy. Consistent sleep timing, avoiding alcohol, and managing how sickness disrupts sleep architecture all contribute to baseline stability.
Living With an Autoimmune Sleep Disorder
The practical reality is harder than the clinical description suggests.
Narcolepsy, for instance, isn’t just sleepiness. It’s the constant calculation of when it’s safe to drive. It’s explaining to an employer why you fell asleep in a meeting. It’s managing cataplexy, learning which emotions to suppress in public because laughing too hard might drop you to the floor.
The social and occupational consequences accumulate alongside the neurological ones.
Comorbid sleep disorders in chronic illness are common and complicate management. A narcolepsy patient who also develops sleep apnea has competing treatment demands. Someone with autoimmune encephalitis may recover their sleep architecture only to struggle with residual cognitive symptoms and anxiety.
The psychological dimension is real. The mind-body connection in autoimmune conditions works both ways: living with an unpredictable, stigmatized condition increases psychological stress, which in turn influences inflammatory tone.
Many people with autoimmune sleep disorders also experience autonomic nervous system dysregulation that affects heart rate, blood pressure, and temperature control during sleep, adding further complexity.
Support groups, particularly condition-specific ones like those organized by the Narcolepsy Network or Wake Up Narcolepsy, offer something clinical care often can’t: contact with people who understand the day-to-day reality. Online communities have expanded access significantly for people in areas with limited specialist coverage.
Autoimmune sleep disorders invert the usual disease logic. Most autoimmune conditions cause pain or organ damage that sends people to a doctor. Here, the attack targets the invisible architecture of consciousness itself, the circuits deciding when you’re awake, dreaming, or paralyzed, meaning the destruction can be nearly complete before anyone thinks to look for an antibody.
The Role of Neurological Sleep Disorders in the Broader Autoimmune Picture
Sleep disturbances don’t exist in isolation. For many people with autoimmune conditions, sleep is the canary in the coal mine, deteriorating before other symptoms become obvious, and improving before other markers respond to treatment.
Neurologically driven sleep disorders share important features with autoimmune presentations: disrupted circadian rhythms, REM abnormalities, and impaired restorative sleep stages. The distinction between a neurological and autoimmune cause often lies in the antibody panel and the treatment response, not in the sleep study itself.
This matters for research as well as clinical practice.
As antibody testing becomes more accessible and the list of recognized pathogenic antibodies grows, conditions currently labeled “idiopathic”, meaning we don’t know the cause, will likely split into subgroups, some of them autoimmune, some not. Idiopathic hypersomnia may well be that territory already.
The broader picture also includes how different sleep disorder categories overlap with autoimmune mechanisms, an area where clinical sleep medicine and neuroimmunology are increasingly converging.
Promising Signs: When Treatment Works
Early immunotherapy, In autoimmune encephalitis, starting IVIG or plasma exchange within weeks of symptom onset significantly improves outcomes, including full sleep-wake cycle restoration in some patients. Sodium oxybate for narcolepsy, Reduces both cataplexy frequency and daytime sleepiness; many patients achieve substantial functional improvement within weeks of reaching therapeutic dosing. Scheduled napping, Strategic 15–20 minute naps timed across the day can reduce reliance on stimulant medication and improve alertness in narcolepsy. Condition-specific support, Engagement with patient organizations correlates with better disease self-management and reduced diagnostic delay in future patients.
Warning Signs That Require Urgent Evaluation
Rapidly progressive psychiatric symptoms with sleep disruption, New-onset psychosis, personality change, or confusion combined with sleep-wake reversal in a young person warrants antibody testing for autoimmune encephalitis, not just psychiatric admission. Cataplexy in any form, True emotion-triggered muscle weakness is not explained by other common conditions and requires urgent sleep medicine evaluation. Total or near-total insomnia, Severe insomnia combined with neuromyotonia, hallucinations, or autonomic instability should prompt testing for Morvan’s syndrome or related encephalitides. Recurrent weeks-long hypersomnia episodes, Episodic hypersomnia with behavioral changes strongly suggests Kleine-Levin Syndrome and shouldn’t be attributed to depression without investigation.
When to Seek Professional Help
A bad night’s sleep is normal. What’s described below is not.
Seek a sleep medicine specialist or neurologist promptly if you experience:
Irresistible daytime sleepiness that doesn’t improve with more nighttime sleep and interferes with work, driving, or daily tasks
Any episode of emotion-triggered muscle weakness, a jaw drop, knee buckle, or collapse while conscious
Sleep paralysis occurring frequently, particularly with vivid hallucinations
Sleep-wake reversal or complete inability to maintain normal sleep timing despite trying
Recurrent episodes of hypersomnia lasting days to weeks, separated by periods of complete normality
New neurological or psychiatric symptoms, confusion, hallucinations, seizures, appearing alongside severe sleep disturbance
Seek emergency evaluation immediately for:
Acute confusion or inability to recognize people or surroundings combined with sleep disturbance
New-onset seizures with any sleep or cognitive changes
Psychiatric crisis, paranoia, hallucinations, or dangerous behavior, particularly with recent infection or fever
If you’re in crisis, contact the 988 Suicide & Crisis Lifeline by calling or texting 988 (US). For neurological emergencies, go to the nearest emergency room or call emergency services.
Specialist resources include the American Academy of Sleep Medicine (sleepeducation.org) for finding accredited sleep centers, and the Autoimmune Encephalitis Alliance (aealliance.org) for condition-specific support and specialist directories.
The United States has openly linked its military actions against Venezuela to control over the South American country’s vast oil reserves after kidnapping President Nicolas Maduro.
US Ambassador to the United Nations Mike Waltz said Monday that Washington would not allow its “enemies” to control major oil reserves, explicitly citing those in Venezuela under Maduro.
“We’re not going to allow the Western Hemisphere to be used as a base of operation for our nation’s adversaries,” said Waltz, less than two hours before Maduro’s first court appearance in New York.
“You cannot continue to have the largest energy reserves in the world under the control of adversaries of the United States, under the control of illegitimate leaders, and not benefiting the people of Venezuela,” the US envoy added.
According to Sami al-Arian, director of the Center for Islam and Global Affairs (CIGA) at Istanbul Zaim University, the US attack and abduction was “a declaration, made through aggression, that sovereignty in the Western Hemisphere is a mirage subject to US intervention – and that international law is an instrument reserved for adversaries and weak states, not an obligation that applies to great powers or empire”.
Waltz denied that the US is occupying Venezuela, even after US President Donald Trump said his administration would be “running” Venezuela.
“There is no war against Venezuela or its people. We are not occupying a country,” Waltz claimed during his speech at the UN Security Council.
Venezuela’s UN ambassador, Samuel Moncada, called the action “an illegitimate armed attack lacking any legal justification.”
Trump has brazenly claimed that Venezuela had “stolen” oil from an industry the US had built “with American talent, drive and skill”, calling it “one of the largest thefts of American property in the history of our country”.
To understand Trump’s actions in Venezuela, Arian says, one must situate them within a larger pattern of imperialism.
“Declared in 1823 by the fifth US president, James Monroe, the Monroe Doctrine sought to establish the Western Hemisphere as a US sphere of control,” he wrote in the Middle East Eye.
“Over time, it evolved into a doctrine of hemispheric enforcement: the US would determine which governments were deemed ‘legitimate’, which were ‘dangerous’ and subject to sanctioning or replacement, and which resources were ‘strategic’ and could thus be acquired by hook or crook,” he added.
Venezuela sits atop more than 300 billion barrels of oil, the largest proven crude reserves in the world, but it’s not just about oil.
Venezuela’s Orinoco mining belt is rich in gold and other precious metals. With more than 8,000 tonnes of gold, the country holds one of the largest reserves in the world.
Trump’s “anti-narcotics” or “anti-corruption” pretexts cited for the intervention carry a hidden purpose – in this case, handing him and the heads of multinational corporations the power to decide who controls concessions, who commands trading routes, and who gets to monetize what lies beneath the ground.
Venezuela also holds billions of tonnes of iron ore and significant deposits of rare earth elements, nickel, copper and phosphates. These resources are critical inputs for modern technology and industrial production, including steel, which is essential for manufacturing military hardware.
In geopolitical competition, control of heavy-industry resources often determines the balance of power.
In the weeks and months preceding the attack, the US tightened the screws on Venezuela in ways that revealed its strategic purpose. Last month, the US imposed a naval blockade that disrupted tanker flows, seized cargoes, and halved oil exports.
What Washington demonstrated was not simply that sanctions inflict harm, but that sanctions, blockades and seizures are deployed as preparatory fire for regime change.
What Washington has sought to reverse is not only where Venezuela’s oil flows, but what that oil is used to build at home.
Following Hugo Chavez’s election as president in 1998, Venezuela redirected oil revenues towards large-scale social programs designed to address decades of extreme inequality.
In the years that followed, poverty was cut by more than half, extreme poverty fell sharply, and access to healthcare, education, housing and food subsidies expanded dramatically.
It was precisely this model that US policy sought to dismantle, beginning with targeted financial measures in the mid-2000s, and escalating after 2015 into sweeping oil, banking and trade sanctions.
The humanitarian deterioration that followed was the direct consequence of a deliberate reversal of social gains through externally imposed economic strangulation, aimed not at reforming governance, but at forcing regime collapse by making the existing system economically unviable.
American energy companies and hedge funds surged Monday following the US military’s abduction of Maduro and Trump’s pledge to “run” the South American country and control its vast oil wealth.
The MSCI US Energy index jumped 2.8 percent, with Chevron leading oil producers up six percent, ConocoPhillips 3.3 percent, and Exxon Mobil 2.4 percent, while oil-field services giant Halliburton soared 10 percent.
Analysts noted that US firms stand to gain not only from the removal of Maduro but also from billions of dollars in contracts supplying equipment and services to Venezuela’s oil industry, a sector largely dominated by US companies before former Venezuelan president Hugo Chavez’s partial nationalization in 2007.
By contrast, European energy firms like BP and Shell remained mostly flat, and Saudi Aramco saw slight losses.
Analysts also warned that if US-backed exploitation of Venezuela’s oil succeeds, OPEC countries, including Russia and Saudi Arabia, could face “serious competition.”
That’s what Kristen Towery, 46, thinks now when she looks back on her symptoms and the nearly two decades it took to get a proper diagnosis.
During her junior year of college, the bout of mono was so bad that she had to miss a semester of classes.
“I never felt like I got fully better,” she says. “I really still struggled with the fatigue. That was something that stuck with me throughout my early twenties.”
For the first few years, Towery visited different doctors, mentioning the fatigue to see if anyone could suggest a solution. “Could I have this chronic fatigue syndrome I keep hearing about?” she would ask, explaining that she just couldn’t get back to normal energy levels.
The fatigue wasn’t completely debilitating at that point. “But I knew that I didn’t really have enough energy to go to work and come home and be the other things that I needed to be,” says Towery, who at the time was working in the corporate buying offices of Neiman Marcus in Dallas. “It was exactly like The Devil Wears Prada. Super super stressful and that took a lot out of me, and not feeling like I had the energy on top of it made it much worse.”
Most doctors blew her off. Chronic fatigue syndrome doesn’t really exist, they would tell her. “You just need to exercise.” “Work less.” “Get more sleep.”
The Pain Starts to Creep In
Throughout her twenties, Kristen endured other seemingly random symptoms here and there. She had pain in her neck that she saw a chiropractor for. She recalls going to several dermatologists for mysterious rashes — “I’d break out in hives from time to time.”
There was one instance with hip pain so piercing that it sent her to the emergency room, but then it went away.
In Kristen’s early thirties she started noticing some pain in her hands and she saw a couple of different doctors. But “it wasn’t enough to drive me crazy,” she says, and she didn’t push.
The First Flare: Could It Be Lupus or RA?
Kristen, who now lives Tampa, Florida with her husband and two Chihuahuas, hadn’t given much thought to the idea that she could have an autoimmune disease. It was the early nineties when she graduated college, and you couldn’t exactly look up your symptoms online.
But then, around seven or eight years ago, she got hit with a bad flu-like illness. “In retrospect, I think it was a horrible flare,” she says. Sick, hot, feverish, with rashes that kept breaking out across her chest, shakiness and loss of balance. “Weird things,” she says.
It was at this point that other people started to suggest to Kristen that she might have lupus. Enter Google — and conviction.
“I started researching it and thought, ‘oh, it has to be lupus,’” says Kristen.
She ruled out RA because “I thought you have to be screaming in pain, that it has to be super bad. I felt like my symptoms leaned more toward fatigue.” The lupus signs, for Kristen, were adding up: hair loss, rashes, brain fog, anxiety issues.
Her primary care doctor had run a slew of RA and Lupus blood tests, found nothing, and told her the five words no chronic illness patient ever wants to hear: “It’s all in your head.”
She pushed for a referral to a rheumatologist.
The rheumatologist agreed that Kristen’s symptoms sounded like they could be lupus, and he ran more tests. Everything, she says, came back negative. Tests that look for certain antibodies in the blood — rheumatoid factor and antinuclear antibody (ANA) — were both negative. (More than 95 percent of people with lupus will test positive for ANA.) Her sedimentation rate, which measures levels of inflammation in the body, was normal.
“You don’t have RA. You don’t lupus,” the doctor told her.
Trying to Get Back on Track
Kristen, who by now had quit her job as a high school English and history teacher because it was way too taxing, was defeated and confused. “I felt half dead,” she says. The brain fog was making it impossible for her to think straight. “I couldn’t get up in front of the class and remember how to spell basic words.”
After taking a break from work, she gradually started feeling better. She went back and got a different teaching job, which was going well… and then she got hit with another flare.
This time, Raynaud’s, a condition in which blood circulation to your extremities becomes limited, started popping up and turned Kristen’s fingers purple. Her back and hips were throbbing.
“I was waking up in the morning with my hands in little claws, and my feet hurt really badly,” says Kristen, who by this time found out that her grandmother had had rheumatoid arthritis.
She felt something shift in her gut — and somehow just knew she had RA too, even if blood tests wouldn’t confirm it. She sought out a different rheumatologist.
Getting Diagnosed: “I Was Almost Giddy”
Kristen told the rheumatologist (who she still treats her today), all about her complicated medical history. This time, though, the radiographic imaging finally caught it. “They X-rayed every bit of me,” Kristen says.
Based on the X-rays, the doctor told her she likely had about five years of damage to her joints. It was rheumatoid arthritis.
Kristen’s reaction to learning she had RA was probably different than the average patient’s. “I was smiling,” she remembers. She was just so relieved to have a name for what she’d been experiencing for almost 20 years — nearly her entire adult life.
What’s more, Kristen’s husband had been living with psoriatic arthritis for 10 years, and was managing it well on a TNF inhibitor biologic. Kristen assumed she too would get on a treatment and start feeling fine.
Adjusting to RA
It wasn’t quite that simple. Now on her fourth biologic, Kristen is finally starting to feel like maybe everything’s under control.
“It’s been a roller coaster up and down, an emotional journey,” she says. “It hasn’t been super easy, but I feel better than a lot of people do and I finally feel like I’m in a place where I’m better able to balance my time and feeling better. I’m getting there. I’m the best I’ve been in a long time.”
As for having a husband who also has inflammatory arthritis? “It was actually a little harder for me in the beginning,” Kristen says. “Because his has been quite well controlled, I think he expected mine to be right off the bat. And mine has been a lot more difficult to control.”
Even while on treatment that controls her pain symptoms well, she still struggles with fatigue, which he husband typically doesn’t.
“I think he expected me to be better sooner,” Kristen says. But over time they’ve seen that their diseases are very different from one another’s and have learned to adjust to it. “And he gives me my shots, so that’s a good thing.”
From Patient to Advocate
“When I was diagnosed I knew pretty quickly that I wanted to get involved in shaping the conversation and the process, beyond the level that was just stuffing envelopes,” says Kristen. “I had been living so long undiagnosed and I wanted to take steps to make sure that doesn’t happen to other people, or lessen the degree to which it does.”
She saw online that CreakyJoints had put out a call for people with RA who would be interested in sitting on a patient council and to fill out an application. “I thought, there’s no way they’re going to pick me — I’m newly diagnosed, I haven’t done any other advocacy work yet. But I filled it out and I got a phone call not too long after.”
Kristen joined our Patient Council for people living with inflammatory arthritis, and has been actively involved ever since.
As a member, Kristen helps inform and shape patient-centered communication and educational materials. For example, she was involved with the development of our Rheumatoid Arthritis Patient Guidelines.
“Education is empowering,” she says. “I’ve had friends who have been diagnosed with diseases like this and not really even take much of an effort to learn themselves about the disease. That surprises me because the more you know, the better your treatment outcome can be. You have to educate yourself and not just rely on what the doctors say. Don’t just trust everything you read online. Read journal articles, read abstracts. Stay up to date on what’s happening and what the different treatment options are.”
“Work with your doctor but don’t necessarily rely 100 percent on them,” she says firmly. “We’re the patient, we have to live with this, and it’s important to take as much of it into our own hands as we can.”
Being part of CreakyJoints has also helped Kristen find the peer support she didn’t know how badly she needed.
“It’s so easy to get in your head and feel like this is only happening to me,” she says. “I didn’t know how to live with this unpredictability or this pain, but when you start to meet other people who do, that’s empowering. Just to know that you’re not the only one.”
If you’ve been having symptoms that you suspect are lupus, or your doctor thinks you might have lupus, you might be Googling like crazy or your mind may spinning with questions: What does this mean for your future? How will you be treated? Will you ever feel healthy/normal again? And just what is lupus, anyway?
Here, we address your basic questions and more.
Lupus is an autoimmune condition
No one is sure what causes lupus, but doctors do know that the symptoms emerge when your immune system isn’t working as it should. Your immune system cells that are supposed to protect the body from different germs start treating normal, healthy cells like invaders, attacking them and causing flare-ups that can affect the joints, kidneys, and almost any other system in the body.
The symptoms of lupus are vague
Symptoms of lupus vary from person to person, from severity to the body parts affected. Some of the most common signs of lupus are a rash and joint pain, says Konstantinos Loupasakis, MD, a rheumatologist with MedStar Washington Hospital Center, but symptoms can also include fatigue, hair loss, mouth sores, and fever. “There’s a great range of manifestations we see with lupus,” he says.
Lupus can be diagnosed at any age
Women at childbearing age (between 15 and 44) are at the highest risk of lupus, according to the Centers for Disease Control and Prevention (CDC), but the disease isn’t limited to younger adults. Between 10 and 20 percent of people with systemic lupus are diagnosed before age 18, according to a study in Nature Reviews Rheumatology, and adults can also have “late-onset” lupus that is diagnosed after age 50.
Race is a risk factor
People of color — particularly African Americans — are at a higher risk of lupus than white people are, and the disease tends to affect populations differently. Native American and black patients tend to have higher mortality rates than white patients, while Hispanic and Asian patients have a lower risk of lupus, according to a study of 42,000 lupus cases. (Read more about stroke risk in black and hispanic lupus patients.) There seems to be a genetic component to the disease, but researchers are investigating how socioeconomics and other factors play into the discrepancies.
Women are at a higher risk
Most studies find that about 90 percent of lupus patients are women, according to a review in Seminars in Arthritis and Rheumatism. The study also found that men tend to have more damage earlier in the disease and have lower survival rates. Hormones might play a role in the sex differences, but studies haven’t found a conclusive answer, says Dr. Loupasakis.
You’ll want to enlist a specialist
The symptoms of lupus are vague and the condition requires regular follow-ups, so a general practitioner will need to refer you to a specialist if he or she suspects an autoimmune problem like lupus. “When there is concern [that you could have] lupus, a rheumatologist should be involved in evaluating this diagnosis,” says Jason Liebowitz, MD, a rheumatology fellow with Johns Hopkins Bayview Medical Center. Once they have a confirmed diagnosis, lupus patients will likely visit their rheumatologist every three months or so, adds Dr. Loupasakis.
A blood test can help, but it isn’t a surefire diagnosis
Because lupus is caused by activity in the immune system, doctors will want to test for certain antibodies to find out what’s happening on a cellular level. Antinuclear antibody (ANA) levels tend to be high in people with autoimmune problems, and about 98 percent of people with systemic lupus test positive to the ANA blood test.
But that doesn’t mean every person with a positive ANA has lupus. With or without lupus, about 14 percent of the general U.S. population shows positive ANA tests, according to a 2012 study, so doctors can’t rely on a single test to diagnose lupus.
A lupus diagnosis is based on symptoms and tests
Without a single blood test clinch a lupus diagnosis, rheumatologists need to look at the whole picture. “There is no single finding that defines the diagnosis of lupus,” says Dr. Liebowitz. “It is a condition that can affect the body in many different ways, and thus diagnosis requires putting together the entire clinical picture.”
When rheumatologists suspect an autoimmune problem, they will take your symptoms into account while looking at X-rays, blood tests, and biopsies to see if results match what they’d expect from lupus, or if it is more likely a different disease.
Lupus can look like other conditions
Other conditions like rheumatoid arthritis, fibromyalgia, and Lyme disease share symptoms with lupus. Without a specific blood test pointing to lupus or other autoimmune conditions, it can sometimes take trial and error for rheumatologists to pin down the right diagnosis.
There is no cure for lupus
At this point, scientists haven’t found a cure for lupus. That said, the chronic disease is not a death sentence. With new medications, lupus mortality rates have improved over time, and the life expectancy for women with lupus-related kidney inflammation is almost on par with women of similar age groups in the general population, according to a study in the Internal Journal of Immunopathology and Pharmacology.
Medications can help
Drugs can’t cure lupus, but they can prevent flare-ups. Available medications can suppress the immune system, holding back the antibodies that would otherwise be triggering inflammation. “The most important treatment for lupus is a medication called Plaquenil [hydroxychloroquine]. Essentially all patients with lupus should be on this medication,” says Dr. Liebowitz. “The other medications used in lupus — which may include mycophenolate mofetil, cyclophosphamide, and other immunosuppressive medications — depend on the symptoms of lupus and the parts of the body that have been affected.” A rheumatologist will be able to recommend the best treatment plan for a particular patient.
Systemic lupus is the most common form
There are several types of lupus, but most people refer to the most common form: systemic lupus erythematosus, also known as SLE or systemic lupus. About 70 percent of people with lupus have SLE, according to the Lupus Foundation of America. Compared to other types of lupus, it tends to be more severe and is more likely to affect a major organ, such as the kidneys, lungs, or heart.
Sometimes, lupus is just limited to the skin
Patients with systemic lupus can have rashes, but some patients have discoid lupus, which means they might only get rashes and skin lesions, rather than joint pain, kidney problems, and other symptoms seen in SLE. About 17 patients with discoid lupus will see their disease turn systemic later, according to a Swedish study in the British Journal of Dermatology, but “most of the time, it will never progress,” says Dr. Loupasakis.
Certain drugs might trigger lupus symptoms
When some people take certain medications, including isoniazid, hydralazine, and procainamide, their bodies can overreact and start showing lupus-like symptoms. Typically, they’ll have symptoms like low-grade fever, aching and swelling joints, or occasionally rashes, but the more serious aspects like kidney inflammation don’t tend to show up, says Dr. Loupasakis.
The condition is separate from “true” systemic lupus because it isn’t chronic. “In the majority of these patients, once they stop the medication, the symptoms will go away in a few weeks,” Dr. Loupasakis says.
Some babies are born with lupus
Sometimes, a mother with lupus or antibodies related to it can pass those antibodies to her newborn, causing a form of lupus called neonatal lupus. “‘Bad’ antibodies are transferred from the mother to the baby along with ‘good’ antibodies that are supposed to protect the baby in the first months of their life,” says Dr. Loupasakis.
Typically, the result is lupus-like skin lesions that go away after a few months, when the babies start to make their own antibodies, he says. In rare cases, the child of a mother with those antibodies will develop a condition known as congenital heart block, but moms-to-be with lupus shouldn’t stress. Only 2 to 5 percent of babies whose mothers have those antibodies will develop congenital heart block, according to a study in Arthritis & Rheumatology. These problems can be detected during ultrasound during pregnancy and babies can be treated immediately after being born by getting a pacemaker implanted to help regulate the electrical activity of the heart.
Lupus can damage the kidneys
Left unchecked, inflammation running rampant in the body can lead to serious complications. For lupus, damage to the kidneys is a big concern. About 40 to 70 percent of lupus patients have kidney inflammation, according to a study in Nature Reviews Nephrology, making renal failure one of the main comorbidities.
“Unfortunately we see that quite often, especially in patients that did not present to us early enough,” says Dr. Loupasakis. The life expectancy of lupus patients with renal disease or failure is three to ten years lower than that of a lupus patient without kidney problems, according to a study of 700 Hong Kong patients.
Lupus also increases cardiovascular risk
Indirectly, lupus can lead to cardiovascular problems. Lupus doesn’t directly affect the heart, but the inflammation the disease causes can speed up the formation of blood clots, says Dr. Loupasakis. Cardiovascular disease is the leading cause of death in people who have had lupus for more than five years, according to a study in Current Cardiology Reviews. One thing you can do to help reduce your risk of heart disease is to eat a healthy, Mediterranean-style diet that focuses on healthy vegetables and seafood while avoiding red meat, recommends Dr. Loupasakis.
Imagine your body is a castle and your immune system is an army fighting off invaders like germs. If the army malfunctions and attacks the castle itself, you may have an autoimmune disease. There’s no cure for autoimmune diseases, but your healthcare provider will help you find treatments that manage the symptoms you experience.
What are autoimmune diseases?
Autoimmune diseases are health conditions that happen when your immune system attacks your body instead of defending it. Healthcare providers sometimes call them autoimmune disorders.
Usually, your immune system is like your body’s built-in security system. It automatically detects substances that shouldn’t be in your body (like viruses, bacteria or toxins) and sends out white blood cells to eliminate them before they can damage your body or make your sick.
If you have an autoimmune disease, your immune system is more active than it should be. Because there aren’t invaders to attack, your immune system turns on your body and damages healthy tissue.
Autoimmune diseases are chronic conditions. This means if you have an autoimmune disease, you’ll probably have to manage it and the symptoms it causes for the rest of your life.
Types of autoimmune diseases
There are more than 100 different autoimmune diseases. They can affect almost any tissue or organ in your body, depending on where your immune system malfunctions, including your:
Joints.
Muscles.
Skin.
Blood vessels.
Digestive system.
Endocrine system.
Nervous system.
This isn’t a complete list of autoimmune diseases, but some examples of conditions (and where they affect you) include:
Autoimmune diseases are common, especially because there are so many different types. Experts estimate that around 1 in 15 people in the U.S. has an autoimmune disease.
What are autoimmune disease symptoms?
Autoimmune diseases can cause a wide range of symptoms. They can affect your body almost literally from head to toe.
For example, conditions that affect your muscles can cause muscle weakness. You might also have joint pain, swelling or feel stiffness if you have a condition like rheumatoid arthritis. Type 1 diabetes causes high blood sugar (hyperglycemia). Some autoimmune conditions affect your vision.
Many autoimmune diseases cause inflammation, which can include:
A feeling of warmth or heat.
Discoloration or redness on your skin.
Swelling.
Pain.
Lots of autoimmune diseases cause symptoms that come and go (recur). These episodes of more noticeable or more severe symptoms are called flares or attacks. Tell your provider if you experience symptoms that seem to recur — especially if certain physical activities, times of day, foods or drinks, or anything else makes them noticeably better or worse.
Trust your gut. Nobody knows what’s normal for your body better than you. Visit a healthcare provider if you notice any new symptoms you can’t explain, especially if you don’t feel like yourself more often than usual.
What causes autoimmune diseases?
Experts don’t know for certain what causes autoimmune diseases. We know your immune system mistakenly damaging your body instead of protecting it causes the symptoms of an autoimmune disease you experience. But researchers are still studying what makes your immune system start hurting you in the first place.
What are the risk factors?
Some studies have found that certain factors (triggers) might increase your risk of developing an autoimmune disease. Some triggers may include:
Viral infections, including COVID-19 and Epstein-Barr virus.
Your sex. Women are more likely to have autoimmune conditions.
Having biological relatives with autoimmune diseases. Some autoimmune conditions are genetic conditions and pass through generations of a biological family.
Having one autoimmune disease can increase the odds of developing another one (multiple autoimmune syndrome).
Exposure to chemicals or other environmental factors (aspects of where you live or work that impact your health) might trigger autoimmune diseases.
Smoking and using other types of tobacco can cause many health issues, including potentially triggering autoimmune diseases.
How do healthcare providers diagnose autoimmune diseases?
Healthcare providers diagnose autoimmune diseases with a physical exam and by discussing your health history. You might also need some tests.
Your provider will examine your body, especially if you’re experiencing symptoms in a specific area. They’ll ask about the symptoms you’re experiencing and when you first noticed them. Tell your provider if you know any of your biological family members have an autoimmune disease.
Diagnosing an autoimmune disease is often a differential diagnosis. This means your provider will test you for several different conditions that can cause the symptoms you’re experiencing until they find the cause.
Your provider might order blood tests to look for specific signs (markers) of autoimmune diseases. These markers are like clues your immune system leaves behind after it damages your body or causes specific issues.
You might need some imaging tests to take pictures of the insides of your body, including:
X-rays.
MRI (magnetic resonance imaging).
CT scan (computed tomography scan).
Ultrasound.
What are autoimmune disease treatments?
Autoimmune diseases can need a variety of treatments. Just like the wide variety of symptoms they cause, which treatments you’ll need depends on which condition you have. Everyone’s immune system, genetics and environment are different. That means the treatments that work for you will be unique.
Some common treatments to manage autoimmune disease symptoms include:
Pain relievers.
Anti-inflammatory medication like NSAIDs or corticosteroids.
Immunosuppressants.
Physical therapy.
Occupational therapy.
IVIG infusions.
You might need specific treatments based on the condition you have. For example, people with Type 1 diabetes need insulin therapy and people with celiac disease need to eat a gluten-free diet.
Can autoimmune diseases be cured?
There’s no cure for autoimmune diseases. They’re chronic (long-term) conditions that usually last your whole life. Some autoimmune diseases enter remission, a long period of time between symptom flares. This isn’t the same as a cure, but it might mean the symptoms impact your daily routine less often.
Can you prevent autoimmune diseases?
There might not be any way to prevent autoimmune diseases because experts aren’t sure what causes them.
How do I take care of myself?
Everyone’s body and journey with an autoimmune disease is different. Talk to your healthcare provider about the best ways to manage the symptoms you experience. You might need to adjust the kinds of physical activities you do, the foods and drinks you consume or make other tweaks to your day-to-day routine.
Is an autoimmune disease serious?
Living with an autoimmune disease like lupus, rheumatoid arthritis and multiple sclerosis can be complex and serious. Although there are no cures for these diseases, many of their symptoms can be treated, and sometimes they go into remission. Stay in touch with your healthcare provider about any advances in understanding and treating autoimmune diseases.
What is the life expectancy of someone with an autoimmune disease?
It’s hard to give an estimate of how an autoimmune disease will affect your lifespan (how long you live). Some conditions are more serious than others, and can cause fatal complications.
Conditions like multiple sclerosis and myositis are more likely to be fatal than many autoimmune diseases, but that doesn’t mean they always are. Similarly, Type 1 diabetes can be fatal if it’s not managed.
Talk to your healthcare provider. They’ll explain how an autoimmune disease will affect your lifespan (if at all).
When should I see my healthcare provider?
Visit a healthcare provider if you’re experiencing new or worsening symptoms you can’t explain — especially if they affect your ability to do all your usual activities.
If you’ve already been diagnosed with an autoimmune disease, tell your provider if it feels like your treatments aren’t working as well as they used to or if the symptoms are recurring more often.
When should I go to the emergency room?
Go to the ER or call 911 (or your local emergency services number) if you experience any of the following severe symptoms:
Trouble breathing or shortness of breath (dyspnea).
Severe chest pain or pressure in your chest.
A headache that starts suddenly and feels unusually serious or intense.
Sudden weakness, especially if you can’t move.
Dizziness that doesn’t stop.
Pain so severe that you can’t stand it.
Which questions should I ask my provider?
You may want to ask your provider:
Which tests will I need?
Is this condition genetic?
What kinds of treatments will manage my symptoms?
How will I need to change my daily routine?
A note from Cleveland Clinic
Finding out you have a health condition that you’ll have to manage for the rest of your life can be overwhelming and scary. It might seem even more unfair if your healthcare providers can’t say what caused it.
Having an autoimmune disease can be hard. And it can be tough for others to understand how much effort it can take you just to move through the world on a day-to-day basis. Give yourself credit for how strong you are. Celebrate small victories, and don’t be afraid to feel frustrated or ask for support from your loved ones and providers.
Autoimmune diseases come in all shapes and sizes. Your healthcare providers will help you find treatments that manage the symptoms you experience. You’re not defined by a condition you have, it’s just a part of your health journey.
Broadway is a major east-west thoroughfare in the city of Vancouver, British Columbia, Canada. In Vancouver’s numbered avenue grid system, it runs in place of a 9th Avenue, between 8th and 10th. The street has six lanes for most of its course. Portions of the street carry the British Columbia Highway 7 designation.
The route begins as “West Broadway” at the intersection of Wallace Crescent and 8th Avenue, in the affluent residential neighbourhood of West Point Grey, a few kilometres east of the University of British Columbia (UBC). Past Alma Street, Broadway takes over from 10th Avenue as one of Vancouver’s major thoroughfares, as it enters Greek West Broadway (or Greektown) section of Vancouver’s Kitsilano district. East of here are several blocks of generally trendy, upscale shops interspersed with low-rise apartment blocks and small supermarkets. The surrounding neighbourhoods generally consist of large, older homes dating from the early twentieth century, many of which have been subdivided into rental suites.
As Broadway approaches Arbutus Street, the commercial establishments become larger before transitioning into a mix of small to mid-size apartment blocks. East of Burrard Street, the apartment blocks get progressively taller, and commercial establishments larger and busier. Between Burrard and Main Street, Broadway can be considerably congested by vehicular traffic. Past Granville Street, Broadway yields completely to medium-to-large commercial structures and high-rise apartments and condominiums. Between Cambie and Main, the commercial establishments become smaller and somewhat more downscale.
At Ontario Street, two blocks west of Main, the route becomes “East Broadway.” After bisecting Main and Kingsway, traffic on Broadway eases somewhat, and the character returns to a mix of small-to-medium apartment buildings and commercial establishments, interspersed with older homes – all considerably less affluent than those to the west. At Commercial Drive, Broadway passes by the Commercial–Broadway SkyTrain Station. Past here for several blocks, the neighbourhood consists predominantly of older residential homes.
As Broadway travels east of Renfrew Street, the neighbourhood once again becomes mixed, with older homes to the north and larger industrial, commercial, and warehouse establishments to the south. Broadway finally ends at Cassiar Street, just short of the Vancouver-Burnaby boundary, where it becomes the Lougheed Highway.
Broadway was created at the turn of the 20th century, along with other gridded roads south of False Creek, to meet the needs of an expanding population in Vancouver. The name of the route was changed from 9th Avenue to Broadway in 1909, at the behest of merchants around Main Street (at that time the hub of Vancouver commerce), who felt that it bestowed a more cosmopolitan air. Commercial establishments originally spread out around the intersections of Cambie and Main Streets, while the character of the rest of the route remained predominantly single-family dwellings.
By the 1970s, the length of Broadway had become a major arterial route in Vancouver, conveying commuters from downtown to the neighbourhoods of the west and east sides. With the growth of UBC and the expansion of the Vancouver General Hospital (one block south of Broadway between approximately Oak and Cambie), traffic demands accelerated. In the 1990s, the agency then responsible for public transit in Greater Vancouver — BC Transit — introduced an express bus route, the 99 B-Line, to help reduce congestion. The Vancouver transportation plan for Broadway notes that congestion is such that the bus service is at capacity, and will not be eased until a new rapid transit line is built paralleling the street. It is anticipated that the SkyTrain’s Millennium Line will be extended to Central Broadway by 2021; the extension is expected to connect with Canada Line at Broadway-City Hall Station, at the intersection of Broadway and Cambie Street.
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