6 Lifestyle Changes to Support Your Autonomic Nervous System
The lifestyle interventions your neurologist actually recommends
There’s a nervous system running your body that you never have to think about. It keeps your heart beating at the right speed. It tells your gut to move food along after a meal. It adjusts your blood vessels so blood reaches your brain when you shift positions. It regulates your temperature, your sweating, your pupils, your bladder.
This is your autonomic nervous system: the body’s autopilot. And when it stops working properly, the effects can be bewildering.
Too tired to read through this article? I get it! Here is a tip sheet.
What is the autonomic nervous system?
The autonomic nervous system (ANS) is the branch of the nervous system that controls everything you don’t consciously decide to do. It has two main arms: the sympathetic nervous system, which revs things up (think fight-or-flight), and the parasympathetic nervous system, which slows things down (think rest-and-digest). In a healthy system, these two arms are in constant, dynamic balance. Your heart rate rises when you exercise and settles when you rest. Your blood pressure adjusts when you stand. Your digestion hums along without you needing to supervise it.
But the autonomic nervous system does something else that most people, even many clinicians, don’t fully appreciate: it helps regulate the immune system.
The vagus nerve is a central player here. Often called the longest cranial nerve, it is a major branch of the parasympathetic (”rest and digest”) system, linking the brainstem to the heart, lungs, gut, and other organs in the chest and abdomen. What surprises many people is that the vagus is mostly a sensory nerve: roughly 80% of its fibers carry information from the body back to the brain rather than the other way around. This gives it a constant, detailed picture of what’s happening inside the body, including signs of inflammation, which it can detect directly.
The vagus nerve is also part of a growing web of communication between the nervous system and the immune system. Through what’s known as the cholinergic anti-inflammatory pathway, this circuit helps dial down the release of pro-inflammatory cytokines, the signaling molecules that drive inflammation. When this system is working well, it acts as a brake on excess inflammation. When vagal tone is reduced, as it often is in people with autonomic dysfunction, that brake may weaken, which has been linked to higher levels of inflammatory markers. This remains an active area of investigation but proof of principle now extends beyond animal models: vagus nerve stimulation reduces inflammatory cytokines and improves disease activity in rheumatoid arthritis in controlled trials.
Farmhouse in Provence, by Vincent Van Gogh, 1888.
What does autonomic dysfunction actually look like?
I’ve written previously about POTS (postural orthostatic tachycardia syndrome), one of the most recognizable faces of autonomic dysfunction. In POTS, the heart rate surges excessively on standing, often accompanied by lightheadedness, brain fog, palpitations, and exercise intolerance. Interestingly, tachycardia (elevated heart rate) may not be the central issue in POTS. Orthostatic cerebral hypoperfusion, or reduced blood flow to the brain when standing, with impaired autoregulation is a well-documented and possibly driving feature of POTS, correlating with its cognitive symptoms and reframing much of the syndrome as a defect of cerebral blood flow rather than a simple consequence of tachycardia.
Here is my tip sheet on how to test for POTS at home.
But POTS is just one presentation. Autonomic dysfunction can show up in ways that patients and often clinicians don’t immediately connect to the nervous system.
Gastrointestinal symptoms are among the most common and most overlooked. When the autonomic nerves that coordinate gut motility are impaired, people may experience gastroparesis (delayed stomach emptying), early satiety, nausea, bloating, constipation, or alternating constipation and diarrhea. These symptoms are frequently attributed to irritable bowel syndrome or stress, and the autonomic contribution goes unrecognized. Recent research has highlighted the bidirectional relationship here: the gut-brain axis is mediated in large part by vagal afferent fibers, and autonomic dysfunction can both cause and be worsened by GI disturbance.
Sweating abnormalities, too much in some areas, too little in others, are a hallmark of small fiber autonomic involvement. Bladder dysfunction, including urinary urgency, frequency, and retention, affects a significant proportion of patients. Temperature dysregulation, feeling intolerably hot or unable to cool down, is another common complaint. Dry eyes and dry mouth can reflect autonomic impairment of the glands that produce tears and saliva. And cardiovascular symptoms beyond POTS, including blood pressure instability and inappropriate heart rate responses, can make everyday activities unpredictable.
The unifying thread is this: autonomic symptoms are not “just anxiety.” They are not psychosomatic. They reflect real dysfunction in the nerve fibers that regulate the body’s most basic operations.
The autonomic nervous system in MS and small fiber neuropathy
In my clinic, I see autonomic dysfunction frequently, in people with multiple sclerosis, in others with small fiber neuropathy, and not infrequently in some who carry both diagnoses.
As we discussed in a previous article: up to 84% of people with MS show some form of autonomic dysfunction, with orthostatic intolerance (intolerance to being upright) affecting around half. Demyelinating lesions in the brainstem and spinal cord can directly disrupt the autonomic pathways that regulate cardiovascular, gastrointestinal, and bladder function. But there’s a second mechanism that doesn’t get enough attention: some people with MS also have small fiber neuropathy, where the tiny nerve fibers that carry both pain and autonomic signals are themselves affected. A growing body of research, including a case series presented by my team at the American Academy of Neurology, has begun documenting this overlap: selected people with MS in whom neuropathic pain and dysautonomia appear traceable to small fiber involvement.
Small fiber neuropathy (SFN) on its own is a driver of autonomic symptoms. The small unmyelinated C-fibers and thinly myelinated Aδ-fibers that are affected in SFN are the same fibers that regulate sweating, blood vessel tone, gut motility, and vascular reflexes that influence heart rate. When these fibers are disrupted or damaged, the clinical picture can include orthostatic intolerance, GI dysmotility, temperature dysregulation, and abnormal sweating alongside the burning pain that often brings patients to clinic in the first place.
What’s important to understand is that these aren’t separate problems. The pain, the autonomic symptoms, the fatigue, they share a common neurobiology.
Six lifestyle changes that support your autonomic nervous system
There is no single medication that fixes the autonomic nervous system. But there is strong evidence, and strong clinical experience, that lifestyle modifications can meaningfully improve autonomic function and reduce symptom burden. They’re not alternatives to medical treatment which can be necessary to mitigate symptoms. For some, these changes may be enough to start feeling better and improve function. For others, medical treatment needs to be sought out first to improve symptoms enough to make these changes possible.
1. Hydration and electrolytes
This is first because it is foundational. Many people with autonomic dysfunction have orthostatic symptoms (symptoms that worsen when standing up such as tachycardia or malaise) due to reduced blood volume leading to reduced blood flow to the brain, and even mild dehydration can dramatically worsen malaise, brain fog, and fatigue.
The goal isn’t just “drink more water,” though in the context of acute symptoms 500cc of water drank fast may do the trick. Otherwise, you need fluid and sodium. The Vanderbilt Autonomic Dysfunction Center, one of the leading clinical programs for disorders of the autonomic nervous system, recommends two to three liters of fluid daily along with increased salt intake, often in the range of 4–6 g sodium per day, equivalent to 10–15 g of table salt (and up to ten grams of sodium for some patients, under medical guidance). Sodium helps retain water in the bloodstream, expanding blood volume, and thus reducing orthostatic symptoms.
Practical strategies include oral rehydration solutions rich in sodium, electrolyte supplements (such as LMNT), salting food liberally, and spacing fluid intake throughout the day rather than trying to catch up in the evening. Talk to your medical team about the right target for you, particularly if you have heart failure, kidney disease, or high blood pressure, where these recommendations may differ or be contraindicated.
2. Movement and exercise done right
Exercise is one of the most effective interventions to support the autonomic nervous system and one of the most misunderstood. Many people with autonomic dysfunction have experienced exercise intolerance or symptom flares that made them understandably wary of physical activity. Deconditioning, in turn, worsens autonomic function: studies show that people with POTS have roughly 16% reduced cardiac mass and 20% reduced blood volume compared to even sedentary healthy controls. It’s a vicious cycle.
What is clear is that structured exercise training works. In a head-to-head trial, a three-month exercise program was compared directly against propranolol; both lowered standing heart rate, but exercise was superior at restoring upright hemodynamics and improving quality of life. And across exercise cohorts, the majority of patients who complete a three-month program no longer meet diagnostic criteria for POTS. The key is how you start: recumbent or semi-recumbent exercise (rowing, recumbent cycling, swimming) that builds cardiovascular fitness without challenging your upright blood pressure and heart rate regulation. Structured programs that combine aerobic reconditioning with resistance training, particularly for the thighs and core, help further maintain venous return. The progression is gradual: reclined to upright, shorter to longer, lower intensity to moderate intensity typically over two to three months.
But there’s an important caveat that doesn’t get enough attention: postexertional malaise. Some people, particularly those with overlapping features of ME/CFS, experience disproportionate symptom worsening after exertion that goes beyond simple fatigue. This worsening is typically not immediate, and is often delayed by hours to a day or more. If that’s you, the standard graduated exercise protocol may need significant modifications, and pushing through symptoms is not just unhelpful, it can be harmful. This is an area of active clinical debate, and the right approach requires careful individualization rather than a one-size-fits-all prescription.
It’s also worth being honest about the challenges. Many individuals feel more fatigued in the first few weeks of a new exercise program before benefits emerge, and dropout rates are high. In my clinic, I try to anticipate this and find that counseling my patients through the early phase is critical. And while exercise meaningfully improves cardiovascular fitness and orthostatic tolerance, it may not resolve all symptoms, particularly headaches, GI dysfunction, or sleep disruption, which often require separate management.
The bottom line: exercise matters enormously, but how you exercise matters just as much. Going too hard, too fast is counterproductive. The goal is a gradual, guided reconditioning program tailored to your specific symptoms and limitations, ideally supervised by a clinician or physical therapist familiar with autonomic disorders.
3. Scheduled recovery
I haven’t shared my personal experience much on this platform, but I live with dysautonomia. I was diagnosed a couple years back but in hindsight, many of my symptoms had been present since my fourth pregnancy, though, like most, I pushed on and ignored them thinking it was my fault I was so exhausted. If there is one change that I made that has helped me navigate the challenges of a dysregulated autonomic nervous system, it is scheduled recovery.
This one is hard. Not because it’s complicated, but because it requires something many of us struggle with: permission.
Recovery is not what happens when you collapse at the end of a day because you’ve run out of energy. That’s a crash, and your autonomic nervous system is already in crisis by the time you get there. Real recovery is planned, protected time, built into your week the same way you’d schedule a medical appointment or a work deadline.
The autonomic nervous system cannot repair and regulate under constant demand. Chronic sympathetic activation, the fight-or-flight state that so many people with dysautonomia are stuck in, doesn’t resolve on its own. It requires deliberate downshifts: periods where the parasympathetic system can take the lead, where vagal tone can recover, where the body gets the signal that it is safe enough to rest.
What does this actually look like? It looks like blocking time on your calendar, not for errands or catching up on email, but for genuine rest. It might be an afternoon with no obligations. It might be a morning where you don’t set an alarm. It might be saying no to a weekend plan that you know will cost you three days of symptoms afterward.
And here’s where it gets uncomfortable: for many people, scheduled recovery requires delegating. It means asking someone else to handle the carpool, the groceries, the household task that you’ve always done yourself. It means letting things be imperfect. It means sitting with the discomfort of not being “productive” and recognizing that rest is productive when your nervous system is the thing that needs repair.
I see this pattern constantly in clinic. Patients who are meticulous about taking their medications, showing up for their infusions, following their exercise programs but who never, ever schedule rest. The guilt runs deep. There’s a feeling that rest has to be earned, that delegating is burdening others, that slowing down is giving in.
It isn’t. It’s treatment. The autonomic nervous system needs recovery time the way a broken bone needs a cast. You wouldn’t feel guilty about wearing a cast. Don’t feel guilty about protecting your recovery.
I found the following article from Chronic Boss particularly helpful in navigating the emotions and identity shifts that rest requires of us living with a chronic illness: here. A worthy read.
4. Nutrition and eating patterns
What you eat and how you eat directly affects autonomic function. Large meals divert blood flow to the gut, which can trigger hypotension, lightheadedness, and fatigue after meals in people with autonomic dysfunction. Eating smaller, more frequent meals throughout the day can prevent this blood pooling effect.
Beyond meal size, dietary composition matters. An anti-inflammatory pattern rich in vegetables, fruits, healthy fats, lean proteins, and fiber, favors a gut microbiome enriched in short-chain-fatty-acid–producing, anti-inflammatory bacteria, whereas heavily processed foods tend to promote pro-inflammatory microbial features. That microbiome is in constant, two-way conversation with the brain along the microbiota–gut–brain axis, in which the vagus nerve is a central relay. But the vagus is just one channel and as a neuroimmunologist, I find it fascinating that this axis also communicates through the immune system. Emerging research increasingly links this system to sleep, stress response, and autonomic regulation, with human studies showing correlations between gut-microbiome patterns and vagus nerve-mediated heart rate variability, though causality isn't yet established. Even with those caveats, feeding a healthy microbiome is more than generic wellness advice; it is increasingly relevant to autonomic health.
If you have gastroparesis or a "slow gut," what you eat may need further fine-tuning. The approach that works best is small, frequent meals that are low in fat and low in fiber, with foods that are soft or well-cooked so they're easier to empty from the stomach. Both fat and fiber slow the stomach down, so they're kept low (not cut out completely). On days when solid food is hard to handle, getting more of your calories from nutritious drinks, smoothies, or soups can help, since liquids go down more easily. Because it's easy to fall short on nutrition, it's worth working with a doctor or dietitian who understands gut and nerve problems.
Alcohol and caffeine deserve a mention. Both affect the autonomic nervous system. Alcohol is a vasodilator that can worsen orthostatic symptoms. My general recommendation is to stay away from it. Caffeine is a bit more personal. While it can temporarily improve alertness, it may also exacerbate tachycardia and anxiety in sensitive individuals. So it's worth seeing how your own body reacts rather than assuming it's off-limits.
5. Sleep
Sleep is when the autonomic nervous system does its deepest restorative work. During healthy sleep, particularly during deep slow-wave sleep, the parasympathetic system predominates, heart rate and blood pressure decrease, and the body shifts into repair mode. Poor sleep disrupts this balance, tilting the autonomic nervous system toward sympathetic dominance: higher resting heart rate, higher blood pressure, greater inflammation.
The relationship runs in both directions. Autonomic dysfunction can fragment sleep (through tachycardia, temperature dysregulation, nocturia, or pain), and poor sleep worsens autonomic dysfunction, creating a self-reinforcing cycle. Breaking this cycle requires deliberate, targeted attention.
The basics matter: consistent sleep and wake times, a cool and dark bedroom, limiting screens before bed, and avoiding caffeine after midday. But for many patients with autonomic dysfunction, standard sleep hygiene isn’t enough. If you’re waking with tachycardia, drenched in sweat, or unable to fall asleep because of pain or restless legs, those problems need to be addressed directly, often with medication. When sleep is genuinely disordered, targeted behavioral interventions like CBT-I (cognitive behavioral therapy for insomnia) have the strongest evidence base of any insomnia treatment.
Emerging research on the gut-brain axis and sleep adds another dimension: the vagus nerve is a key mediator of the signals between gut and brain that regulate sleep architecture. Supporting vagal health through the other interventions on this list may have downstream benefits for sleep as well.
6. Mental health support
I want to be clear about why this is on the list. It is not because autonomic symptoms are “all in your head.” It’s because autonomic dysfunction and mental health exist in a well-documented bidirectional relationship, each one potentially making the other worse through shared neurobiological pathways.
Anxiety activates the sympathetic nervous system. Chronic sympathetic activation lowers heart rate variability, which in turn can amplifies the cardiovascular impact of anxiety. Depression contributes to autonomic imbalance through inflammatory and neuroendocrine pathways. And the hypervigilance that commonly accompany chronic illness can impair vagal recovery.
This is not a character flaw but neurobiology. And it means that treating anxiety and depression isn’t just about feeling better emotionally, it may improve autonomic regulation.
What does this look like in practice? It might mean therapy, particularly approaches with evidence for chronic illness populations, such as CBT or acceptance and commitment therapy. It might mean medication, carefully chosen with attention to autonomic side effects. It might mean peer support, mindfulness practices, or stress reduction techniques that support parasympathetic tone. The key is recognizing that mental health is not separate from physical health in autonomic disease: it is part of the same system.
The big picture
None of these six changes works in isolation. Hydration supports exercise tolerance. Exercise improves sleep. Sleep supports mood. Mood affects gut function. Gut health influences vagal tone. It’s a system and when you support one part of it, the benefits ripple outward.
The same is true of the team around you. Your neurologist, your cardiologist, your PT, your therapist, they’re each supporting a different piece of the same nervous system. The lifestyle changes in this article are the connective tissue between those appointments: the daily, weekly, ongoing work that no one can do for you, but that everyone on your team should be helping you sustain.
If you’re living with autonomic dysfunction, whether from MS, small fiber neuropathy, or another cause, you don’t have to do everything at once. Pick one area. Start small. And build from there.
In your corner,
Dr. Freeman
Relevant References
Benarroch EE. Autonomic nervous system and neuroimmune interactions: New insights and clinical implications. Neurology. 2019 Feb 19;92(8):377-385. doi: 10.1212/WNL.0000000000006942. Epub 2019 Jan 16. PMID: 30651384.
Tesser JRP, Crowley AR, Box EJ, June JP, Wickersham PB, Valenzuela GJ, Gaylis NB, Lam GKW, Pacheco LA, Ridley DJ, Pinto-Patarroyo GP, Novack SN, Churchill MA, Kohler M, Lee EC, Pando JA, Parris GR, Peterson JR, Shah T, Singhal AK, Vuong V, Levine YA, Evangelista ML, Derosier AA, Curtis JR, Richardson RM, Chernoff D. Vagus nerve-mediated neuroimmune modulation for rheumatoid arthritis: a pivotal randomized controlled trial. Nat Med. 2026 Jan;32(1):369-378. doi: 10.1038/s41591-025-04114-7. Epub 2025 Dec 22. PMID: 41429981; PMCID: PMC12823386.
Seeley MC, O'Brien H, Wilson G, Coat C, Smith T, Hickson K, Casse R, Page AJ, Gallagher C, Lau DH. Novel brain SPECT imaging unravels abnormal cerebral perfusion in patients with postural orthostatic tachycardia syndrome and cognitive dysfunction. Sci Rep. 2025 Jan 28;15(1):3487. doi: 10.1038/s41598-025-87748-4. PMID: 39875497; PMCID: PMC11775248.
Koutsouraki E, Theodoros K, Eleni G, Marianna K, Areti N, Ariadni K, Dimitrios M. Autonomic nervous system disorders in multiple sclerosis. J Neurol. 2023 Aug;270(8):3703-3713. doi: 10.1007/s00415-023-11725-y. Epub 2023 Apr 21. PMID: 37084150.
Terkelsen AJ, Karlsson P, Lauria G, Freeman R, Finnerup NB, Jensen TS. The diagnostic challenge of small fibre neuropathy: clinical presentations, evaluations, and causes. Lancet Neurol. 2017 Nov;16(11):934-944. doi: 10.1016/S1474-4422(17)30329-0. Erratum in: Lancet Neurol. 2017 Dec;16(12):954. doi: 10.1016/S1474-4422(17)30361-7. PMID: 29029847.
Robbins NM, Golden EP, Freeman KC, Bhavaraju-Sanka RK, Snapper H, Cook GA. Approach to Postural Orthostatic Tachycardia Syndrome. Neurol Clin Pract. 2026 Jun;16(3):e200620. doi: 10.1212/CPJ.0000000000200620. Epub 2026 Apr 28. PMID: 42114076; PMCID: PMC13155696.
Garland EM, Gamboa A, Nwazue VC, Celedonio JE, Paranjape SY, Black BK, Okamoto LE, Shibao CA, Biaggioni I, Robertson D, Diedrich A, Dupont WD, Raj SR. Effect of High Dietary Sodium Intake in Patients With Postural Tachycardia Syndrome. J Am Coll Cardiol. 2021 May 4;77(17):2174-2184. doi: 10.1016/j.jacc.2021.03.005. PMID: 33926653; PMCID: PMC8103825.
Wang Z, Luo Y, Zhang Y, Chen L, Zou Y, Xiao J, Min W, Yuan C, Ye Y, Li M, Tu M, Hu J, Zou Z. Heart rate variability in generalized anxiety disorder, major depressive disorder and panic disorder: A network meta-analysis and systematic review. J Affect Disord. 2023 Jun 1;330:259-266. doi: 10.1016/j.jad.2023.03.018. Epub 2023 Mar 11. PMID: 36914118.
Chronically low ferritin levels for someone who cannot absorb iron through the gut can be a significant contributor. Iron infusions can be very helpful.