Understanding the Relationship Between Dysautonomia and Lyme Disease

Dysautonomia and POTS in Lyme Disease

Dysautonomia, a dysfunction of the autonomic (involuntary) nervous system, can manifest in various ways. POTS, characterized by a significant increase in heart rate upon standing without a drop in blood pressure, is one of the most common forms of dysautonomia observed in Lyme patients1. Symptoms of POTS include lightheadedness, fainting, tachycardia, fatigue, and difficulty concentrating. These symptoms can severely impact daily activities and quality of life, making accurate diagnosis essential.

Overlapping Symptoms

Many symptoms of POTS and Lyme disease overlap, making diagnosis challenging:

• Fatigue
• Cognitive difficulties (“brain fog”)
• Dizziness and lightheadedness, particularly with position changes
• Exercise intolerance
• Headaches
• Sleep disturbances
• Abdominal pain, nausea, or bloating
• Heart palpitations or rapid heart rate, especially when standing.
• Temperature intolerance, including sensitivity to heat and cold.

This similarity in symptoms can lead to misdiagnosis or delayed diagnosis of either condition (1).

The Infection Connection

Many patients report the onset of POTS following an infection, suggesting a potential link between infectious diseases and the development of this syndrome. Several types of infections have been implicated, including:

1. Viral Infections: Viruses such as Epstein-Barr virus (EBV), influenza, and SARS-CoV-2 have been associated with POTS. These infections can trigger an immune response that may lead to autonomic dysfunction.
2. Bacterial Infections: Lyme disease, caused by the Borrelia burgdorferi bacterium, has been linked to POTS. The bacterial infection may lead to neurological symptoms, including those seen in POTS. Other bacteria implicated in the development of POTS includes Bartonella, Strep, Mycoplasma and many others.
3. Other Infections: Gastrointestinal infections and other infections caused by various pathogens, including parasites like Babesia have also been reported to precede the onset of POTS symptoms.

It is important to note that there are other environmental and toxic exposures that can trigger POTS include hormonal fluctuations, mast cell activation syndrome, stress, trauma, head injury, mold exposure, chemical exposure and underlying autoimmunity such as Celiac disease or Sjogren’s Syndrome.

Mechanisms of Infection-Induced POTS

Several mechanisms have been proposed to explain how infections might trigger POTS:

1. Autoimmune Response: Infections can provoke an autoimmune response, where the body’s immune system mistakenly attacks its own tissues, including those involved in autonomic regulation. This autoimmune mechanism is a key area of research in understanding POTS.
2. Direct Nervous System Impact: Some infections can directly affect the nervous system, leading to inflammation or damage to autonomic nerves. This can disrupt normal autonomic function and contribute to the development of POTS.
3. Chronic Inflammation: Persistent inflammation following an infection or during an infection can lead to autonomic nervous system dysfunction. Chronic inflammation may alter blood volume regulation, vascular tone, and heart rate control. Pelvic Congestion Syndrome (PCS) and May-Thurner Syndrome are compression syndromes that in some cases involves inflammatory processes (that may be infection driven) leading compression of the iliac vein by the iliac artery (or other compressions in the pelvis) which ultimately leads to poor blood flow and can manifest as POTS.
4. Molecular Mimicry: Pathogens may share structural similarities with host tissues, leading the immune system to attack both the pathogen and the body’s own cells. This process, known as molecular mimicry, can contribute to the development of autoimmune conditions, including POTS.
5. Mast Cell Activation Syndrome (MCAS): Mast cells, in response to various infections or toxins, release inflammatory mediators that can lead to an inflammatory response in the autonomic nervous system, causing or exacerbating the symptoms of POTS. They also increase vascular permeability which can affect blood volume and distribution resulting in impaired blood flow and abnormal heart rate responses upon standing, contributing to the orthostatic intolerance and cardiovascular symptoms characteristic of the syndrome. In addition, there are hormonal contributions to POTS that both infections and mast cells can impact. For a range of symptoms and signs of MCAS: https://drtaniadempsey.com/clinical-manifestations-of-mast-cell-activation-syndrome-by-organ-systems/

Clinical Implications

Understanding the link between infections and POTS is crucial for several reasons:

• Diagnosis: Recognizing a history of recent infection can aid in the diagnosis of POTS and help distinguish it from other forms of dysautonomia or cardiac conditions.
• Treatment: Identifying an infectious trigger may inform treatment strategies, including the use of immunomodulatory therapies or targeted antimicrobial treatments.
• Prevention: Awareness of this connection may lead to preventive strategies in susceptible individuals, particularly following infections known to trigger POTS.

Diagnosing Postural Orthostatic Tachycardia Syndrome (POTS)

Proper diagnosis of POTS is crucial for managing symptoms and improving patient quality of life. This article provides a comprehensive guide on how to diagnose POTS effectively.

Diagnostic Criteria

The primary diagnostic criteria for POTS include:

1. Heart Rate Increase: An increase in heart rate of 30 beats per minute (bpm) or more within 10 minutes of standing (40 bpm in adolescents) without significant orthostatic hypotension (a drop in blood pressure).
2. Symptom Duration: Symptoms must persist for more than six months.
3. Absence of Other Causes: Other causes of tachycardia and orthostatic intolerance, such as dehydration, hyperthyroidism, or anemia, should be ruled out.

Diagnostic Process

The diagnostic process typically involves several steps:

1. Detailed Medical History and Symptom Assessment: Gather a comprehensive history starting at birth through current age. Focus on symptom onset, duration, and severity. Evaluate for factors that might exacerbate symptoms and act as triggers such as heat, exercise, food or prolonged standing. Evaluating for MCAS, especially when there are additional symptoms suggestive of mast cell activation is critical.
2. Physical Examination: Conduct a thorough physical examination to rule out other potential causes of symptoms
3. Active Stand Test or Tilt Table Test: These tests are essential for diagnosing POTS. During the active stand test, the patient’s heart rate and blood pressure are measured while lying down and then again after standing. The tilt table test involves the patient being tilted to an upright position while measurements are taken.
4. Blood Tests and Other Investigations: Tests should be performed to exclude other conditions like thyroid disorders, adrenal insufficiency, or anemia. Additional tests should include an evaluation for Mast Cell Activation Syndrome and Vector-Borne Infections. Additional testing could include autonomic function tests and echocardiography.
5. Holter Monitor or Event Monitor: These devices record heart rhythms over an extended period, providing data on heart rate changes and helping to rule out other arrhythmias.

Treatment of POTS

Treatment for POTS usually involves a combination of lifestyle changes, dietary modifications, and medications to manage symptoms and improve quality of life. Treating the root cause is equally important. Some common approaches include:

1. Lifestyle Changes:
   1. Increase salt and fluid intake to improve blood volume and circulation- some patient needs 8-10grams of salt a day.
   2. Compression garments (such as stockings) to improve blood flow.
   3. Gradual changes in posture to avoid sudden shifts in heart rate.
   4. Physical therapy and exercise tailored to the individual’s tolerance level to improve circulation and cardiovascular fitness.
   5. Dietary changes to consider include following a lower carb diet to balance blood sugar and insulin levels, which can impact the nervous system.
2. Medications Options (may vary depending on the patient):
   1. Beta-blockers regulate heart rate but also lowers blood pressure
   2. Fludrocortisone to help retain sodium and increase blood volume.
   3. Midodrine to constrict blood vessels and raise blood pressure when needed.
   4. Pyridostigmine increases parasympathetic nervous system activity and decreases heart rate in POTS Clonidine can stabilize heart rate and blood pressure in patients with high sympathetic nervous system activity.
   5. Ivabradine slows the heart rate without affecting blood pressure.
3. Mast Cell Targeted Therapy- If MCAS is identified as a contributing factor to POTS, targeted treatments such as antihistamines, mast cell stabilizers, and anti-inflammatory medications may help alleviate symptoms. Personalized treatment plans that address both conditions can improve patient outcomes.
4. Treatment of Infections: Once an infection, a vector-borne infection or other bacteria, virus, parasite or fungus is identified antimicrobial treatment should be considered to target the root cause of the autonomic dysfunction.

Conclusion

Infections can play a significant role in the onset of Postural Orthostatic Tachycardia Syndrome, likely through mechanisms involving autoimmune responses, direct nervous system impact, mast cell activation syndrome and chronic inflammation. Continued research into this association is essential to improve our understanding of POTS and to develop more effective diagnostic and therapeutic strategies. Awareness of the potential link between infections and POTS can help clinicians better manage and support affected patients.

Final Thoughts

I would encourage patients to be persistent at getting to the root cause, and even if they know they have Lyme it is important to identify other factors, including other infections, toxin exposures, and other triggers that can be associated. POTS can be debilitating, but it is treatable, controllable and potentially reversible with the right intervention.

–Dr. Tania Dempsey, Founder of AIM Center for Personalized Medicine.

About The Author

Dr. Tania Dempsey is a world renowned expert in chronic disease, autoimmune disorders, and mast cell activation syndrome, and is sought after internationally for her knowledge of chronic immune dysregulation.

As founder of the AIM Center of Personalized Medicine, Dr. Dempsey uses functional and integrative medicine to get to the patient’s root cause(s) of illness, understand why people get sick, help patients understand their body, and understand why it fails them when it does. She works with patients all over the United States, as well as from places around the world such as Israel, England, Thailand, and France.

Dr. Dempsey’s extensive knowledge and experience in Mast Cell Activation Syndrome, mold, and Lyme Disease, has propelled her to the forefront of the functional medical community as a recognized and trusted speaker, researcher, advocate, and physician.

Attending, speaking, and hosting summits, seminars, webinars, podcasts, and conferences are a routine part of Dr. Dempsey’s academic and professional regimen. As a trusted expert, Dr. Dempsey is committed to furthering her knowledge of clinical care, as well as helping other physicians better understand the scope and the possibilities available through functional medicine.