Part 1 of a 3-part series on anxiety, depression, and PTSD
If you live with anxiety, you already know it doesn’t stay in your head. It can show up as a racing heart before you’ve even registered what you’re worried about. Tight shoulders that never quite release. A stomach that won’t settle. Sleep that won’t come, or doesn’t hold.
Anxiety may start as a brain state, but it doesn’t stay contained there. This is the relationship between anxiety and the nervous system: the brain’s stress response recruits other systems in the body, the cardiovascular system, the digestive system, the musculoskeletal system, pulling them into the response whether they were part of the original problem or not.[1] Understanding why it spreads that way is the first step toward addressing the root cause instead of just managing the symptom.
The Brain Is Tracking More Than You Think
Here’s something most people don’t realize: your brain isn’t only responding to what you’d call “stress” in the emotional sense. It’s constantly monitoring three distinct categories of stress: mental/emotional, physical, and chemical. All three contribute to your overall state of mind, whether or not you’re consciously aware of them.
Mental and emotional stress is the obvious one: deadlines, conflict, worry, uncertainty. Physical stress includes things like poor sleep, old injuries, postural strain, or overtraining. Chemical stress includes inflammation, blood sugar swings, toxin exposure, and gut dysfunction. Your brain doesn’t file these into separate categories the way we do. It treats all three as input, and it mounts a stress response that recruits the systems needed to deal with each one: cardiovascular, digestive, immune, musculoskeletal, bringing them “into the fold” to respond accordingly.[1]
This is why anxiety so rarely stays confined to “just feeling anxious.” If the input is coming from three different directions, the output can show up across just as many systems.
What’s Actually Happening in an Anxious Body: Anxiety and the Nervous System
Take the mental/emotional trigger as an example, since it’s the most familiar starting point. Anxiety has a physiological signature. When the brain perceives a threat, real or not, the amygdala fires a distress signal to the hypothalamus, which: which activates the sympathetic nervous system: heart rate up, heart rate up, breathing shallow and fast, muscles tense, digestion paused.[2] This is the body’s ancient survival wiring. It’s designed for the occasional emergency, followed by a return to baseline.
For a lot of people, that return never fully happens. The stress response stays dysregulated, and the nervous system starts treating a normal Tuesday like a threat.[3] Over time, this chronic activation changes how the brain processes fear, and it keeps the body locked out of the parasympathetic “rest and digest” state it needs to actually recover. In anxiety, this overactivation of the stress axis tends to normalize when the anxiety itself resolves, which is part of why the state can be retrained rather than simply endured.[4]
Old Stress, Current Stress, Perceived Stress: The Body Doesn’t Always Know the Difference
Here’s something important to understand about the stress response: it doesn’t only fire in response to what’s happening right now. It can be triggered by stress that’s old: unresolved, stored, still influencing the nervous system long after the original event has passed. It can also be triggered by stress that’s entirely perceived, meaning there’s no real threat present at all, but the nervous system has become sensitized and is now reacting to milder and milder inputs as though they were significant.
Old, current, or perceived, the label doesn’t change what’s happening physiologically. The stress response is a measurable neurobiological event. It can show up in brain states, using tools like QEEG and fMRI. It can show up in physiological markers like blood oxygen saturation (SpO2%) and heart rate variability (HRV). It can show up physically, in muscle tone. And it can show up chemically, in markers of inflammation. It’s a pattern that can show up across multiple independent systems at once.
Like any other pattern the body runs repeatedly, it can become learned. The behaviors and physiological responses that make up someone’s stress response aren’t fixed. They’re acquired, the same way any other habit is acquired. That matters, because what’s learned can also be unlearned or retrained. It also means the pattern doesn’t just go away on its own once it’s established.
The Stress Response Was Built for Short Emergencies
It’s worth remembering what this system is actually for. The stress response is meant to protect you from real danger. The fight-or-flight mechanism is built to handle emergencies that are relatively short in duration. When a new threat appears, you’re meant to enter a state of heightened awareness and do one of a few things: stop what you’re doing (freeze), defend yourself (fight), or change course entirely (flee). All three responses are designed to help you immediately. Once the immediate danger has passed, the job shifts. Now the task is figuring out what you might need to do differently to stay safe long-term.
That’s the design. Short, intense, situational, followed by resolution.
Here’s where it gets more complicated: you don’t need to personally experience a threat to learn to fear it. Witnessing someone else in danger, or even hearing or reading about a danger, is enough for the nervous system to encode a fear response, even if you never actually encounter that threat yourself.[5]
Anticipation Is Your Best Survival Tool, Until It Isn’t
This is where anticipation comes in, and it’s worth understanding because it’s genuinely one of the most powerful tools your nervous system has. The ability to anticipate a problem before it happens lets you modify your behavior in advance, which means you can handle stress and challenges far more efficiently than if you had to wait and react in the moment. Anticipation, at its best, is a survival advantage.
Anticipation only works as intended when it leads somewhere: when it results in a behavior modification that actually addresses the anticipated problem. When anticipation is allowed to run without that follow-through, when the mind plays the same worry over and over, prompting a stress response again and again with no resolution and no behavior change, that survival tool has turned into something else. That’s anxiety.[6]
This is one mechanism behind anxiety, not the whole picture. There are other well-documented mechanisms behind this same state, and as this series develops, I’ll bring those in alongside the clinical and research literature that supports them.
Why the Root Cause Matters More Than the Symptom
This is where I think a lot of anxiety treatment falls short. Managing the symptom, the racing thoughts, the physical tension, the sleepless nights, is necessary. It’s not the same as addressing why the nervous system is stuck in that state to begin with.
In my practice, I look at anxiety as a downstream signal of an upstream dysregulation. A few of the patterns I see most consistently:
Nervous system regulation. The spine houses the communication highway between brain and body. When there’s dysfunction along that pathway, the nervous system has a harder time shifting out of sympathetic dominance and into a calmer, parasympathetic state, even when the “threat” has passed.
The stress-inflammation loop. Chronically elevated stress hormones don’t just affect mood. They drive systemic inflammation, and inflammation in the brain itself can affect the very regions responsible for regulating fear and emotional response.[7] This is part of why anxiety so often travels with brain fog, fatigue, and difficulty concentrating. It’s inflammatory.
Liver and detoxification load. The body’s ability to clear stress hormones and inflammatory byproducts matters. When that clearance pathway is overburdened, the nervous system stays exposed to higher circulating levels of the very chemicals driving the anxious state, a cycle that can make anxiety feel like it’s escalating on its own. (This one reflects my clinical model more than settled research.)
What We Actually See on Brain Function Testing
This is where anxiety stops being an abstract description and starts being something we can measure:
On QEEG (quantitative EEG) testing, we look at how the brain responds to a known, controlled stimulus: a series of light flashes or tones. These are called evoked potentials: auditory evoked potentials (AEP) for sound, visually evoked potentials (VEP) for light. The stimulus is benign and the “correct” response is known. What we can often see in anxious brains is an oversized response relative to the stimulus. The brain is shown two or three flashes and reacts as if it were shown six or seven.[8] Anxiety is also associated more broadly with a pattern of cortical hyperarousal on QEEG.[9] The reverberation that follows measures out in milliseconds, but it’s there, and it’s measurable.
There’s an important nuance to this: an anxious response in a naturally slow-processing brain looks different from an anxious response in a naturally fast-processing brain. Anxiety in a fast brain can be a more disruptive phenomenon, with more reactivity and less built-in buffer.
We also see this pattern on a test called TOVA, the Test of Variables of Attention. Patients are shown a simple sequence of targets and non-targets and asked to respond only to the target. What can show up in anxious patients is a pattern of commission errors: the brain jumps ahead, tries to anticipate what’s coming next, and responds before it should.[10] It’s a brain that’s gotten locked into a pattern where it doesn’t know how to slow down and wait for the actual information. (In the research this association is real but not universal, so I treat it as a clinical observation, consistent with what I’ve seen across thousands of these tests, rather than a settled rule.)
To be clear: we don’t diagnose anxiety from either of these tests. Clinical diagnosis follows established guidelines. QEEG and TOVA give us observation: objective, measurable insight into how a person’s brain is actually wired and how it behaves under a controlled load. Given how much anti-anxiety medication is prescribed, and how rarely people get to actually see what’s happening in their own nervous system, that observation matters. The goal is to equip people with real information about how their brain works, so they understand what they’re dealing with instead of just managing a label.
Where Anxiety and Depression Start to Overlap
One more thing worth understanding, especially if you’ve ever wondered whether what you’re dealing with is anxiety, depression, or some combination of both: the two are far more connected than the separate diagnostic labels suggest.
Brain imaging research increasingly shows that mood and anxiety disorders share overlapping circuitry. The same fronto-limbic regions involved in fear, emotion, and self-regulation, including the prefrontal cortex, amygdala, insula, and anterior cingulate, show altered activity across both conditions.[11] Anxiety and depression, in other words, often aren’t two separate problems so much as two points on the same continuum.
Here’s the mechanism as I see it in practice. An anxious brain that stays “on” indefinitely is spending resources it doesn’t have unlimited access to. Run that pattern long enough, the same thoughts, the same loop, no real modification in behavior, and the brain eventually has to make a choice. It starts to burn through its own metabolic resources, and that depletion is one of the more common contributors to depression.
On QEEG, I often see this as a specific combination: high anxious brain activity paired with low metabolic brainpower. The anxiety, in a very real sense, can be the thought process that leads there.
That’s the thread I’ll pick up in the next post: depression as a multisystem condition, metabolic, behavioral, perceptual, and physical, and where it diverges from, and grows out of, what we’ve covered here.
What This Means for Treatment
Anxiety that’s rooted in nervous system dysregulation, chronic inflammation, and impaired detoxification doesn’t resolve by addressing only the mind. It requires an integrated approach: one that considers the spine, the gut, the liver, and the brain as a connected system, not four separate problems.
This is the model I use with patients with anxiety: identify where the dysregulation is actually coming from, physiologically and, when relevant, in measurable brain function, and address that, instead of only managing what may show up on the surface.
In the next post in this series, I’ll walk through depression through this same lens: where an anxious brain can burn through its own resources and tip into a depressive pattern, and what that means for how the two conditions are treated differently.
If you’re dealing with anxiety that hasn’t responded to conventional approaches alone, this integrated model may explain why, and what a different starting point could look like.
Recovery, resilience, and clarity, they all have a biology.
At Well Rooted Health, mindfulness and recovery are understood through the lens of nervous system function. How you regulate stress, process experience, and restore capacity is connected to how your body is working at a foundational level. Every new patient relationship begins with a comprehensive physical exam, in Westfield NJ, New York City, or virtually.
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References
- Chan KL, Poller WC, Swirski FK, Russo SJ. Central Regulation of Stress-Evoked Peripheral Immune Responses. Nature Reviews Neuroscience. 2023;24(10):591-604. doi:10.1038/s41583-023-00729-2.
- Benarroch EE. The Amygdala: Functional Organization and Involvement in Neurologic Disorders. Neurology. 2015;84(3):313-24. doi:10.1212/WNL.0000000000001171.
- Russell G, Lightman S. The Human Stress Response. Nature Reviews Endocrinology. 2019;15(9):525-534. doi:10.1038/s41574-019-0228-0.
- Juruena MF, Eror F, Cleare AJ, Young AH. The Role of Early Life Stress in HPA Axis and Anxiety. Advances in Experimental Medicine and Biology. 2020;1191:141-153. doi:10.1007/978-981-32-9705-0_9.
- Müllner-Huber A, Anton-Boicuk L, Pronizius E, et al. The Causal Role of Affect Sharing in Driving Vicarious Fear Learning. PLoS One. 2022;17(11):e0277793. doi:10.1371/journal.pone.0277793.
- Merino H, Senra C, Ferreiro F. Are Worry and Rumination Specific Pathways Linking Neuroticism and Symptoms of Anxiety and Depression in Patients With Generalized Anxiety Disorder, Major Depressive Disorder and Mixed Anxiety-Depressive Disorder? PLoS One. 2016;11(5):e0156169. doi:10.1371/journal.pone.0156169.
- Koo JW, Wohleb ES. How Stress Shapes Neuroimmune Function: Implications for the Neurobiology of Psychiatric Disorders. Biological Psychiatry. 2021;90(2):74-84. doi:10.1016/j.biopsych.2020.11.007.
- Baas JM, Milstein J, Donlevy M, Grillon C. Brainstem Correlates of Defensive States in Humans. Biological Psychiatry. 2006;59(7):588-93. doi:10.1016/j.biopsych.2005.09.009.
- Wang H, Mou S, Pei X, et al. The Power Spectrum and Functional Connectivity Characteristics of Resting-State EEG in Patients With Generalized Anxiety Disorder. Scientific Reports. 2025;15(1):5991. doi:10.1038/s41598-025-90362-z.
- Ciftci E, Alp ZB. Quantitative EEG Insights Into A Hundred Adult ADHD Patients: A Deep Dive Into Test of Variables of Attention (TOVA) Correlations and Attention Dynamics. CNS Neuroscience & Therapeutics. 2025;31(3):e70304. doi:10.1111/cns.70304.
- Janiri D, Moser DA, Doucet GE, et al. Shared Neural Phenotypes for Mood and Anxiety Disorders. JAMA Psychiatry. 2020;77(2):172-179. doi:10.1001/jamapsychiatry.2019.3351.