Gait Testing Can Predict Future Post Concussion Syndrome

A recent study in the journal Gait and Posture looked at various biomarkers in posture and walking in athletes who suffered a #concussion.⁣

⁣Prognosis for Persistent Post Concussion Symptoms using a Multifaceted Objective Gait and Balance Assessment Approach


They wanted to see if any specific findings on balance or gait testing could predict which patients would have a worse recovery.⁣

The study found that out of all of the balance and walking parameters, 2 metrics were associated with the development of persistent symptoms or #postconcussionsyndrome


𝗗𝘂𝗮𝗹 𝗧𝗮𝘀𝗸 𝗮𝗻𝗱 𝗚𝗮𝗶𝘁⁣
The study found that when concussion patients had to perform a cognitive task while walking, there were changes in their walk that predicted future symptoms.⁣

Patients that were more likely to have future symptoms showed 𝙞𝙣𝙘𝙧𝙚𝙖𝙨𝙚𝙙 𝙢𝙤𝙫𝙚𝙢𝙚𝙣𝙩 𝙤𝙛 𝙩𝙝𝙚𝙞𝙧 𝙡𝙤𝙬𝙚𝙧 𝙗𝙖𝙘𝙠 when walking, and also 𝘀𝗵𝗼𝘄𝗲𝗱 𝗺𝗼𝗿𝗲 𝗿𝗮𝗻𝗱𝗼𝗺 𝗳𝗼𝗼𝘁 𝗽𝗹𝗮𝗰𝗲𝗺𝗲𝗻𝘁 when landing when they were engaged in a cognitive task.⁣

This might not seem like a big deal, but this may be a subtle sign that the brain is struggling to compartmentalize basic movement patterns, so it is using important resources from the frontal lobe to do something as simple as walking straight.⁣

This is why we have all of our patients perform a walking test with and without a cognitive challenge.⁣

The dual task paradigm gives us insight into brain function, and it also lets us know if we can use dual task exercises like the Fitlight to enhance our rehab.⁣

#neuroscience#neuroplasticity#tbi

Occipital Neuralgia – Migraine-like Pain without the Migraine

A sharp and sometimes electric nerve pain coming from the back of the head that can radiate over the top of the skull or into the eyes.⁣

The pain from occipital neuralgia can be severe, and is often misdiagnosed as a #migraine.⁣

While occipital neuralgia is common after a head injury like #concussion, it can come out of nowhere from tight neck muscles or inflammation to a nerve called the greater occipital nerve.⁣

These types of headaches can be resistant to most medications, but can be alleviated by addressing mechanical factors in the neck, especially in the #atlas of the upper cervical spine.⁣
While there is no definitive test to diagnose occipital neuralgia, we can often find a tender point in the back of the head/neck that can reproduce the pain. That along with a detailed health history can help us identify the source of the head pain so it can be treated properly.⁣

The Dangers of Stroke

This post hits close to home, but it’s so important that lay people understand the signs and risk factors for stroke.

As a chiropractor trained heavily in neurology, I’ve spent years understanding and training to recognize when someone may be having a stroke. Despite my training, my wife suffered multiple strokes over the course of 3-4 days, and I was only able to catch the largest and most recent one.

Survival and recovery from stroke heavily depend on early recognition and treatment, and depending on the location of the stroke, a matter of minutes can mean the difference between life and death.

Signs of Stroke
The most common signs involve looking for facial dropping, arm weakness, and speech issues.

However, other serious signs include alterations in consciousness/awareness, nystagmus, and unsteadiness in walking and balance.

What makes stroke unique from other problems is that these signs will present suddenly and out of nowhere.

You can also combine the signs and symptoms with a patient history of risk factors.

Big risk factors are any history of high blood pressure, artery disease, and heart disease.

Important risk factors for stroke

Also be aware if someone is taking medications like blood thinners or birth control which can contribute to stroke risk.

Lastly, a recent history of infection or a recent autoimmune flare up can increase risk of stroke.

Strokes can be scary, and it can be terrifying to see a loved one show these signs. However, it is survivable and can be treated when recognized and treated early.

After the acute threat of stroke is over, a plan for comprehensive neurological rehabilitation can drastically improve a survivor’s life.

Is Your Neck Muscle Connected to Your Heart Muscle?

Is Your Neck Muscle Connected to Your Heart Muscle?

A 2015 study suggests that it might be the case. At least in rats.

Neck muscle afferents influence oromotor and cardiorespiratory brainstem neural circuits

The authors of the study were evaluating the anatomic mechanisms for how whiplash disorders and dystonia could cause problems with facial, oral, and cardiorespiratory issues.

To do that, they applied electrical stimulation to the upper neck muscles of rats and used molecular tracing techniques to identify what areas of the brain were stimulated.

They found that stimulating the upper neck muscles had unique pathways into an area in the brainstem called the nucleus intermedius, which had a direct impact on breathing and heart rate in the mice.

Even more interesting was that stimulating the neck muscles had as strong an effect as stimulating that area of the brain stem directly!

This effect was also specific to neck muscle stimulation, as pure sensory fibers didn’t produce the same effect. The effect was also not reproduced when stimulating nerves from the lower neck.

Obviously we don’t know for sure if this happens in humans because this was a rat study after all.

But studies like these might help explain why doing an adjustment to the upper neck seems to elevate vagus nerve function as measured by heart rate variability. It might also explain why many of our patients with #potssyndrome and other forms of #dysautonomia have had success with NUCCA.

The science on this is still very young, but it’s exciting to see the anatomical connections that make the upper neck such an important area to work on.

Inflammation: Friend or Foe

Last week I gave a talk to a group about the role of your immune system in pain and inflammation.

It’s easy to forget that the immune system that is responsible for fighting germs and illness is the same immune system that produces the inflammation that heals sprained joints or causes arthritic joint pain.

Acute inflammation vs chronic inflammation

It’s also easy to forget that inflammation in of itself is not good or bad. It’s a response from specific cells and systems in the body in response to a perceived threat.

While chronic inflammation can have negative effects on your heart, arteries, and brains, we need acute inflammation to help heal from injuries and to fight off infectious diseases.

A key lynchpin to an appropriate immune and inflammatory responses goes back to the brain and nervous system.

Acute inflammation acts like a reflex not much different than when a doctor taps on your knee to see if it kicks. If you have a cut or scrape, your immune system will kick into gear to wall that area off from germs and create heat and swelling and there’s nothing you can do about it. It’s embedded into our physiology.

These responses allow your body to clean up and repair damaged tissue while also containing germs trying to get in and invade the body during injury. Acute inflammation can be painful and uncomfortable, but it is a marvelous example of how we evolved to survive injury.

On the flip side, chronic inflammation is a maladaptive response where the body’s immune system isn’t shut down. It can occur in a variety of ways including:

  1. An underlying infectious process is never fully dealt with
  2. The presence of antibodies that attack the body’s own tissues (Lupus, Grave’s Disease, Rheumatoid Arthritis)
  3. A dysregulated stress response
  4. Inappropriately primed immune cells from brain injury or gut barrier problems

These processes can predispose people to a higher risk of heart disease, stroke, diabetes, and cancer, on top of just not feeling well on a day to day basis.

In order to beat the causes of chronic inflammation, we have to address the reasons that body creates inflammation.

It’s through this understanding that we have the ability to help address some of the chronic inflammation that leaves us susceptible to the chronic diseases of aging.

Vestibular Migraine – When the Brain Causes Dizziness

Vestibular migraine (VM) is a condition in which dizziness and vertigo can occur from central brain changes that occur similar to migraine headaches.


Although VM has #migraine in its name, it can happen with or without the feeling of a migraine headache. Some patients have just #vestibular symptoms like #vertigo. Others will have both #headache and vertigo along with other neurological manifestations.

VM is the most common cause of episodic vertigo, but it is frequently misdiagnosed for other inner ear disorders.

The hallmark signs of VM are a history of migraine headaches and increased visual dependency in balance.

Even when not in the midst of a vertigo attack, patients with VM can have debilitating imbalance and motion sickness between episodes and are persistent.

The good news is that many cases are treatable with migraine treatments like migraine meds, anti-CGRP antibody therapies, and vagus nerve stimulation seem to reduce attacks.


Between attacks, cervical and vestibular rehab can help decrease the burden of persistent imbalance and dizzy symptoms.

This is a place where functional neurology and upper cervical care really thrives.

Check out our most recent VM patient and you can see significant decreases in their disability scores and big improvements on their balance and sway.

Meniere’s Disease: A Craniocervical Solution

Meniere’s Disease (MD) is a debilitating illness with a lot of unknowns about it’s true nature. This misunderstanding has led to a lot of MD patients getting ineffective or excessively damaging treatments on patients that are desperate for relief. It’s also an illness that tends to be misdiagnosed by a lot of clinicians unless you have substantial experience working with dizzy patients.

So how do you know if you have a true Meniere’s Disease versus other vestibular disorders, and what are your options once you do know that you have Meniere’s?

Meniere’s Disease vs Other Vestibular Disorders

Meniere’s Disease is part of a spectrum of disorders called vestibular disorders. Vestibular disorders consist of any illness that affects the inner ear system that controls your sense of balance and equilibrium.

Examples of vestibular disorders include:

  • Benign Paroxysmal Positional Vertigo (BPPV)
  • Vestibular neuritis
  • Vestibular migraine
  • Mal de Debarquement
  • Central vestibulopathy (stroke or brain injury)

Diagnosing vestibular disorders can be challenging because there’re so many things that can cause dizziness.

Meniere’s Disease is defined by vertigo that comes out of nowhere (episodic), hearing loss, ringing in the ears (tinnitus), and a clogged feeling in the ears (aural fullness).

When we compare Meniere’s to other disorders, the closest diagnosis has to be vestibular migraine because of it’s episodic levels of vertigo. It’s also challenging because there is a large overlap in patients with Meniere’s having a history of migraine headaches [Source]

The defining characteristic with Meniere’s Disease when you compare it to other vestibular disorders is hearing loss and auditory symptoms, specifically the feelings of fullness in the ears.

If you have vertigo and dizziness, but you don’t have hearing loss with auditory symptoms, then you do not have Meniere’s Disease.

Difficulty Treating Meniere’s Disease

Another key component with Meneire’s Disease is the fact that it is notoriously difficult to treat. While other vestibular disorders like BPPV and vestibular neuritis can be treated successfully with Epley Maneuvers and vestibular rehabilitation, these procedures are not beneficial for patients with Meniere’s.

A big reason is that Meniere’s Disease can come in the form of flare ups. So while patients with Meniere’s can get some benefit from doing vestibular and balance training between flare ups, they will often regress hard when a flare up occurs again.

The timing and frequency of flare ups is unique to each patient. Some may experience flare ups on a weekly basis while others can go months between episodes. Each flare up does tend to worsen auditory symptoms which is even more distressing.

Medications like Beta Histadine may provide some benefit between flare ups but generally doesn’t affect hearing. Recommendations for a low sodium diet appear to provide some relief in reducing episodes, but compliance to the diet is poor.

Furthermore, there aren’t any good therapies that affect the auditory symptoms. The constant feeling of fullness in the ear and the roaring tinnitus persist and get worse. Currently, only steroid or gentamyicn injections have been used for some patients, but outcomes are hit or miss.

Patients who are at their wits end may get surgical decompression of the vestibular organ, or choose to cut nerve in the ear in hopes to get relief. This comes with the price of hearing and vestibular loss for the affected ear.

Craniocervical Care

Anecdotal evidence from chiropractors focusing on the upper neck have given many with Meniere’s hope for some improvement. Dozens of case reports show that adjustments to the upper cervical spine have given patients relief in both the vestibular and auditory symptoms related to Meniere’s Disease.

Dr. Michael Burcon out of Michigan began a clinic specifically for treating patients with Meniere’s Disease and published outcomes on 300 patients with the disorder. [Source]

Over the course of 6 years, he reported a large improvement across 300 patients with most improvements occurring by 6 weeks. He also noted that many MD patients could identify a whiplash trauma to the neck about 15 years before symptom onset suggesting the cervical injury may play a role in people with a genetic disposition to Meniere’s.

How the neck influences Meniere’s is currently unknown. There’s suspicion that the upper cervical shift may distort function of the autonomic nervous system causing dysfunctional flow of blood and cerebrospinal fluid. The strong contributions of the upper cervical spine to the vestibular system is also a mechanism for how the neck can influence the dizziness and vertigo symptoms.

While these cases are anecdotal, the improvements that Meniere’s patients have with cervical focused chiropractors is compelling enough and safe enough for patients with MD to explore given the fact that other options are less safe and provide marginal benefit.

Understanding and Treating Persistent Motion Sickness

Patients with persistent motion sickness represent a subset of patients commonly associated with dizziness and imbalance. While many patients with motion sickness have it in relationship with a condition like migraine, vestibular migraine, or BPPV, there are many patients who just struggle with it on it’s own without a complaint of dizziness.

Motion sickness isn’t an illness where you feel a false sense of motion like vertigo. Motion sickness is a problem that different types of motion or perception of motion will cause you to feel nauseated and sick. The difference between these concepts makes a big difference in how you will need to be treated.

Historically it has been a challenge to diagnose and treat these patients because traditional tests of dizziness and imbalance are going to be negative. Without a strong understanding of motion sickness, it becomes difficult to provide treatments or therapies that have enduring effectiveness, and all you are left with are anti-nausea medications.

Patients with motion sickness can feel ill along a wide variety and intensities of motion. The most common form of motion sickness occurs in people who have difficulty riding in boats or cars. A large portion of the population has experienced motion sickness when riding in a rocking boat or attempting to read in a car.

In it’s more severe forms, patients can feel sick with small amounts of head movement, or when exposed to a busy visual background. The feeling of sickness can cause progressive nausea that can eventually lead to vomiting.

What Drive Motion Sickness

As you can tell, being so sensitive to motion that small head movements or visual stimuli can induce vomiting can feel quite limiting and debilitating for a patient. I personally hate the feeling of nausea more than I hate pain, and it’s common for these patients to avoid social events and gatherings so they can feel safe in the comfort of home.

What happens in the body to generate this terrible feeling?

Most of our understanding of motion sickness stems from our knowledge of nausea and vomiting. Nausea can be driven directly by sensation from the vestibular organ or the gut. Neurological signals from the inner ear and the gut travel to the lower brainstem called the medulla where there are specific neurons dedicated to vomiting.

Diagram showing the inputs to the medulla that activate vomiting.

When these neurons are activated, they activate pathways that increase the production of saliva, take deeper breaths, and initiate contractions of the esophagus and diaphragm. That feeling is also triggering the sympathetic nervous system causing blood flow changes that can lead your hands to get cold and you start to sweat.

Remember that this is a pathway for vomiting. Many patients aren’t going to go through this entire process, but the brain regions associated with this process probably contribute to the levels of nausea people have with motion sensitivity.

Nausea and motion sickness can be driven by different sensory stimuli, but all inputs are likely driving sickness through the medulla.


Based on this knowledge, we have sense that patients with persistent motion sickness and nausea may have problems in these regions which serve as targets for treatment or rehabilitation:

  • Vestibular dysfunction – especially the otolithic organs
  • Gut dysregulation
  • Brain driven sensory sensitivity

Sensory Mismatch and Motion Sickness

The exact mechanisms for how motion sickness triggers the above neurological pathways is currently unknown. The most common theory that I’ve found to have practical treatment implications is called the Sensory Mismatch or Sensory Conflict theory.

The theory suggests that you have 3 systems in your body that help you detect if you are in motion. These are the:

  • Visual System
  • Vestibular System
  • Proprioceptive System

Under most circumstances, your brain takes information from these senses and compares it to the brain’s expectation for motion.

Let’s say that you’re going for a run. Your eyes detect movement of the background while you’re running, your muscles detect motion of your joints, your ears detect the bobbing motion of your head, and your brain knows what it is supposed to feel like to go for a run. When these senses all agree and your brain recognizes how this is supposed to feel , then your brain doesn’t have to resolve any conflict and motion feels perfectly fine.

In patients with motion sickness, the information coming from these senses might be weighted different by the brain. What does that mean? It means that your brain may be more sensitive and prioritize the information that comes from your eyes more than the information that comes from your vestibular system or vice versa.

Now your brain has a problem. Your visual system might be saying that you’re moving a lot while your vestibular and proprioceptive systems aren’t perceiving any motion (Kind of like driving in a car right?). Your senses are conflicting, so your brain has to make the final call.

If your brain doesn’t have good information for how this is supposed to feel, then the sensory mismatch isn’t resolved and the conflict leads to you activating the pathways that drive nausea. The most common expression of this is called vestibular-visual mismatch, and is likely the driving force in nausea and motion sickness in vestibular migraine.

When 2 of your sensory systems are in conflict, it’s up to the brain to reconcile the difference. If it fails, you get dizzy. If it succeeds, you are able to adapt.

How does this help us treat patients with motion sickness?

By understanding the influence that these sensory systems play in motion sickness, we can use a careful examination of these systems to determine where and how to provide different therapies.

In my office, we test eye movements, ocular misalignment, balance, and optokinetic responses to assess the way the brain responds to different sensory conditions.

Once we have an idea of how a patient’s senses might be betraying them, then we can move into a treatment strategy to fix it. First we would try to re-weight their sensory system, then we slowly expose the patient to the offending stimuli.

What does this look like as an example?

The majority of patients we have seen with motion sickness have a high level of visual dependency meaning that they rely too strongly on visual information to maintain balance.

If you have high visual dependency then your brain places too much emphasis on detecting visual motion. If this is the case, you can be watching a movie with a busy action sequence and your brain is going to think that you are moving despite the fact that your vestibular and proprioceptive systems say that you are sitting still.

So if we know that the patient is way too visually dependent, then we would have the patients perform exercises to increase their ability to rely on vestibular and proprioceptive senses. That means we might do a lot of their exercises or therapies with their eyes closed initially and gradually progress them to doing exercises with eyes open. As they can tolerate these motions better, then we might slowly start to expose them to the busy visual environments that would normally induce dizziness.

It can be complicated and nerve racking to confront motion sickness because patients with this problem have spent so much time designing their life to avoid these nauseating activities.

But at the end of the day if we are really going to give people their lives back, then we need to have the courage to confront the things that have kept us in the prison of our perceived broken bodies.

Stress, Heart Rate Variability, and the Immune Response to Infection

On our last post, we got familiar with a lot of the players of the immune system. If you missed that post and want to catch up with some of the main cells involved with immunity, you can check it out here:

A Brief Tour of Your Immune System

At the end of the article, I talked about the connection point between the nervous system and the immune system. While it seems like the nervous system and the immune system are mostly separated because of minimal direct nerve connections to immune organs, the brain actually exerts a large influence on immune function.

This is a critical piece to consider because the immune system left to its own devices can simply obliterate an infection with an uncontrolled immune response. This isn’t useful to the organism if an uncontrolled immune response ends up creating widespread tissue damage or killing its host in the process. It would be like setting your house on fire because you saw a roach in your garage.

One easy example is seen with control of a fever. During an infection, your immune system releases a variety of chemicals that will increase your body temperature to slow down the growth of bacteria. The hypothalamus of your brain keeps your body temperature between 98-99 degrees Fahrenheit under normal circumstances. But when an infection occurs, these immune chemicals will raise your body temperature, but the hypothalamus is monitoring your body systems to make sure it doesn’t get too high.

Fever is an example where communication between the immune system and the brain help fight infection while limiting damage to the body.

If your body is getting overwhelmed then your body temperature may continue to rise above 103 degrees and cause harm to your own body systems. This is generally a nuclear option that the brain tries to avoid, so there has to be a delicate balance in allowing your body temperature to rise a little bit while neural feedback will trigger inflammation reduction when temperature rises too high.

This is all mediated through a branch of the nervous system known as the autonomic nervous system.

Stress and the Immune System Relationship Status: It’s Complicated

Your autonomic nervous system mediates your response to stress. Your fight or flight system is activated by the sympathetic nervous system, which is countered by the rest and digest function of the parasympathetic system.

I used to be under the simple belief that stress from a fight or flight response suppressed your immune system because it caused your adrenal glands to release cortisol, and cortisol generally reduces white blood cell count and we end up catching more colds. [Source]

Just like everything else, it seems to be more complex than that.

It’s true that people who are chronically stressed out tend to get sick more often and have lower white blood cell counts. It’s also true that patients under with chronic stress are more prone to autoimmunity and hypersensitivity reactions like rheumatoid arthritis and asthma.

So how do we reconcile the fact that stress can reduce your immunity leaving your more susceptible to infection AND leave you prone to illnesses of a hyper-aggressive immune response?

A super insightful paper published in the Journal Neuroimmunomodulation brought this concept to light. The answer might be in the timing and context of the stress response.

It appears that if you are lightly stressed from exercise or acutely stressed during something that gives you an adrenaline rush, your immune system actually gets a surge of immune cells into the blood. From an evolutionary perspective this makes sense right?

If you are fighting or escaping danger, there is a high likelihood that you will have some sort of injury that will expose your blood to wounds and pathogens. You want more immune cells in your blood to get ready to fight. Your adrenaline-based stress hormones (epinephrine and norepinephrine) tell your immune organs to release more white blood cells into circulation. This also causes a drop in monocytes and lymphocytes, and an increase in neutrophils which would seem that you are evolutionarily preparing your innate immune system. [Source]

At the tail end of a stress response, you want to turn the immune cells down, so as your body releases cortisol, this causes a decrease in immune cell production to reduce the opportunity for autoimmunity. You also get a boost of activity from your vagus nerve which turns on an anti-inflammatory reflex to calm the body back down and reduce inflammation by your immune system. [Source]

However, cortisol also triggers a redistribution of the cells in your blood to go into your tissues to wait for any germ challenges that show up in the skin, lungs, or digestive tract. While this can keep the immune cells armed at the sources of common infection, a cycle of chronic stress that continues to dump immune cells into these battleground locations has the potential to prime these locations for autoimmune disease [Source].

Dhabhar described this as the Barracks to Boulevard to Battleground mechanism for how stress mobilizes the immune system. [Source]

The Barracks to Boulevard to Battleground analogy proposed by Dhabhar https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3412918/

Adrenaline in acute stress tells your spleen, thymus, and bone marrow to “mobilize the troops” from their barracks and get on the road to the battle. This means there are loads of white blood cells on the boulevards (blood stream) ready to go to wherever the battle is going to be. At the end of the stress response, cortisol and other corticosteroids maneuver the white blood cells into battle ground tissues like the skin, lungs, and digestive tract that are likely to engage with potential invaders.

We end up in a situation where just a little bit of stress increases immune responsiveness and increases resistance to infection and cancer which is great!

But chronic stress induces hormone signaling that can reduce white blood cells in the blood stream and into tissues. If you are chronically stressed and dumping more soldiers into your tissues, there can be a risk for autoimmune reactions. At the same time, chronic activation of the stress response is reducing troops in the blood which leaves you prone to other infections.

How acute vs chronic stress can change the way the immune system functions. Acute stress may increase immune protection but can increase hypersensitivity reactions. Chronic stress can suppress the immune system or shift neuroendocrine function to dysregulation

What this likely means is that you don’t have widespread immune suppression from a stress response. In fact, a little bit of stress from things like exercise or being involved in something exciting may actually increase immune protection.

Even chronic stress isn’t necessarily immune suppressive. What chronic stress likely does is redistribute your immune cells to other bodily tissues. Chronic stress is also likely to drive hormone dysregulation which can trigger immune dysregulation leading to the double whammy of increased infections and increased autoimmunity.

Can Heart Rate Variability Tell Us About Our Immune Response?

Now we know that stress can modify our immune response via our autonomic nervous system, can measuring stress tell us about our immune response?

Maybe.

A measurement called Heart Rate Variability (HRV) is a tool we can use to measure your your body’s baseline stress response. I’ve written a lot of thoughts about HRV here.

Long story short, a high HRV score generally tells us that we are have more parasympathetic physiology (less stressed), while a low HRV score generally tells us that we are more Sympathetic physiology (more stressed).

Heart Rate Variability and Stress

If we are under chronic stress, you are generally going to have lower HRV and a stronger likelihood for stress related illness. It’s shown a strong ability to predict outcomes in cancer and stroke, but it also can tell us if a healthy person is more likely to get injured during exercise.

Heart rate variability is generally tied to the function of the Vagus nerve and the parasympathetic nervous system. An extensive amount of work has been done studying something called the cholinergic anti-inflammatory pathway which is driven by the Vagus nerve.

We know that the vagus nerve plays a role in driving inflammation down, and it’s probably a key piece in what helps us get back to normal after the immune system has fought a war with an infection. This anti-inflammatory pathway is how the vagus nerve tells the immune system to calm down and it has been studied extensively in terms of autoimmune, cariovascular, and metabolic disease associated with inflammation. [Source]

We need vagus/parasympathetic physiology to help us balance out the effects of chronic stress, and HRV seems to be a good and cheap way to let us know if it’s working.

But……

Can a stress reading from HRV tell us anything about our ability to fight infection?

Surprisingly not that much research has been published in this space, but here’s some of what has been studied:

  • Low HRV is a predictor for death from sepsis across several studies [Source] It’s unknown whether lower HRV was caused by sepsis, or if lower autonomic capacity allowed for worse disease progression
  • Low HRV scores predicted the progression of disease in patients with hand,foot, and mouth disease from enterovirus infection. Lower HRV scores corresponded with higher organ system involvement [Source]
  • HRV scores in healthy adults showed correlations with increased inflammatory bio markers and lower white blood cell counts in those with lower HRV. [Source]
  • Low HRV after predicted patients who would suffer infection after stroke [Source]
  • Loss of sympathetic modulation identified on HRV was associated with worse outcomes in community-acquired pneumonia patients [Source]
  • Lower HRV in healthy adults shows a slight shift in immune cells towards neutrophils while higher HRV is associated with more lymphocytes [Source]

Taken altogether, it appears that people with better outcomes from a disease process when they have a higher HRV score. However, we don’t really know if HRV is the chicken or the egg. Did the people with poorer outcomes have a better baseline autonomic function or did someone with a worse infection just wipe out that patient’s autonomic nervous system resulting in poor outcome.

We don’t have answers to that quite yet, at least not from clinical research on infectious disease, but maybe something else can give us a clue.

HRV and Cancer

Besides infectious disease, the immune system is heavily involved in eliminating and controlling the spread of cancer cells. Your body is constantly producing mutated cells during the process of normal cell reproduction, but the vast majority of these mutated cells are eliminated by a healthy immune system.

The relationship between stress, heart rate variability, and cancer has been studied really extensively. So much so that there are multiple systematic reviews suggesting that heart rate variability is a strong measurement to assess a cancer patient’s progress in fighting the disease. [Source] One study even suggested that HRV was more reliable in predicting the prognosis of prostate and colorectal cancer than knowing what stage of cancer the patient had. They also found that the more advanced stage you had, the more important vagal activity was in survival, which is a finding consistent in metastatic cancer cases. [Source] You can read more My thoughts about that particular paper below.

Research: Active Vagus Nerve Predicts Cancer Survival Regardless of Stage

Just stop and think about that for a second. The thought that you can crunch the data from a patient’s heart rate and you can tell who is going to have a better outcome in 6 months with all other factors kept equal. It gives us hope that having a better stress response and higher HRV is a driving factor in protection from cancer and not just the product of cancer’s affect on the autonomic nervous system.

Me reading these papers about HRV and cancer

Decouck et al in a 2018 review in the Journal of Oncology explored the concept of vagus nerve activity in cancer even further. Instead of just looking at the studies that measured heart rate variability, they included studies that observed the effect removing the vagus nerve had on cancer progression.

In most animal models, an experimental vagotomy showed higher rates in cancer and worse rates of metastasis implying that a loss of vagus nerve function was causative in developing cancer in mice. We can’t really do these experiments in humans, but we can follow patients who have had their vagus nerve cut in the case of a disease like ulcers. Patients who had a partial vagus nerve removal had higher odds of developing cancer in the organs that lost their vagus nerve connection.

Patients who had a partial vagus nerve removal had higher odds of developing cancer in organs that became disconnected from the nerve.


Do we know if the vagus nerve removal means that there’s less immune surveillance in defending against tumor cells?

Not really.

The effects of the vagus nerve on human physiology are wide spread, so we don’t have any experiments that inform us on this.

But, but but….There are theories.

My favorite looked at the effect that stress and depression had on immune function the progression of cancer.

Stress and depression-induced immune dysfunction: Implications for the development and progression of cancer

Stress and depression’s role on the HPA axis results bias the immune system to an immune response that decreases activation of natural killer cells and cytotoxic T-cells which are responsible for controlling the spread of tumors. Maria E. Et al. International Review of Psychiatry 2005.

Chronic stress and major depression disorder are associated with reduced cellular immunity which is the branch of your immune system that can destroy infected or mutated cells. This response is mediated by Natural Killer Cells in your innate immune system, and T-Cells in your adaptive immune system. These cells patrol your body looking for tissue that has been infected by a virus or has mutated leading to cancer.

They work by binding to the infected or mutated cell and provide a chemical signal for that cell to self-destruct so it can’t spread.

A review of how Cytotoxic T-cells eliminate infected viral threats. Similar mechanisms occur for Natural Killer Cells of the Innate Immune System.

These cells have been found to be reduced or less active in patients who with untreated depression as well as patients and caregivers with prolonged mental health symptoms related to traumatic events.

These cells are so potent in addressing tumor activity in laboratory models that Immunotherapy for cancer is looking at how to harness T-cells and NK cells in treating active cancer patients. [Source]

So Here’s What we know:

  • We know that chronic stress and depression affect heart rate variability negatively.
  • We know that chronic stress and depression are associated with worse or dysregulated immune responses.
  • We know that chronic stress can increase cancer rates via persistent activation of the HPA axis.
  • We know that cancer patients generally have worse HRV and vagal nerve activity than healthy controls.
  • We know that cancer patients with higher HRV have better prognosis and survivability than cancer patients with low HRV.
  • We know that autonomic activity is related to vagal nerve activity which has immune consequences.

We discussed how we couldn’t be sure if having better autonomic function was the cause or the effect of better outcomes with infectious disease, so we couldn’t be certain that having a better autonomic nervous system in a healthy person could protect us from infectious disease.

But we know that cancer survivability is a product of better autonomic function, then it’s my personal contention that building up your autonomic nervous system is a causative factor in having better immune function against infectious illness.

Can We Improve our HRV and Does It Matter?

This article has gone on way longer than I anticipated, but before I close let’s discuss if therapies to improve autonomic function to stress have any potential value.

So the last question we have to ask ourselves is this. Can we change the output of our autonomic nervous system and vagus nerve and does it really matter?

It’s nice to know that having a high HRV gives you greater resilience and survival to disease, but it’s not helpful if some people are just born and raised to have better autonomic control than others. But if HRV can be improved, and that improvement leads to better outcomes, then it gives us tools to improve our lives across multiple dimensions.

Here’s the good news. At least in short term studies, we have tremendous power over our autonomic nervous system. Many of which are free with various mind-body therapies, and others that utilize practitioners of drug-less healing.

Here are some things that have some evidence for improving heart rate variability that also have carry over into improving general quality of life. I’ve highlighted as to whether they can be done free at home, or whether they require outside help or purchase:

  • Free: Systematic review of yoga shows promise for improving Heart Rate Variability [Source]
  • Free: Tai-Chi and Tai Chi/yoga for stress reduction [Source]
  • Paid Apps/Therapists: HRV Biofeedback Training reduces markers of inflammation in asthma, heart disease, and depression [Source]
  • Clinically guided or purchased device: Noninvasive Auricular vagus nerve stimulation reduced depression [Source]
  • Free: Employee based Mindfulness training and meditation improves HRV along with overall life and job satisfaction [Source]
  • Free: Medium intensity exercise improves HRV and patient outcomes across a wide spectrum of chronic illness [Source]
  • Clinically delivered: Upper cervical spine manual techniques [1, 2, 3]

Closing Thoughts

As you look through those sources, you’ll notice that none of those studies really talk about immune function. All this tells us is that improving HRV is possible, and it seems to help us live a better life when we do it.

We can’t measure whether we have optimized our immune system because we have no clue what markers tell us if our immune system is optimized. We know when our immune system is broken, and we know when it is deficient. That’s it.

But we can measure and improve on the function of our autonomic nervous system, and we can do it on the cheap.

Healthy immune function isn’t the goal of improving our autonomic function. It is a potential product of a healthy autonomic nervous system.

We are improving our autonomic function because it is a necessary part of being a healthy human being. Healthy immune function is a product of doing things that we know we should be doing already.

It’ about taking care of yourself mentally.

It’s about building a physical body that is prepared to take on stress.

It’s about ensuring that the function of our nervous systems are not obstructed.

We can’t stop the world from being infected at this point, but we can build a resiliency that will allow ourselves a better chance to fight off disease so we can move on to protect others.

In times of stress, we often forget that we have power and we have control over our lives. During this pandemic, not only do we feel powerless, but we are more afraid than ever. Not just of this invisible virus, but of our fellow human beings.

This fear, this anxiety, this depression that we feel collectively is taking away one of our body’s best weapons to endure our invisible enemy.

In one sense, it’s our immune system, but in another sense it’s something deeper. It is the power human beings discovered when we realized that we are way better fighting together as a village, than as an individual alone in the wild.

While it’s up to experts smarter than I am to give us the best chance to avoid illness, it’s up to us as people to confront this threat without the panic and fear that will not only make us sick physiologically, but will make us a sick species by stripping us of our collective humanity.