If you have POTS, you have probably been told that your racing heart is the problem.

You stand up. Your heart rate climbs. You feel lightheaded, weak, shaky, breathless, nauseated or exhausted. You may experience palpitations, headaches, exercise intolerance, digestive symptoms and brain fog. You may have even passed out, known medically as syncope.

But the fast heart rate is not the root cause. It is a rescue response.

When the blood vessels do not constrict and relax appropriately, when blood pools away from the heart, when circulating volume is inadequate or when blood flow to the brain falls, the heart speeds up in an attempt to maintain circulation.

Sadly, and catastrophically, most cardiologists ask, “How do we slow the heart rate?” But the root-cause question is: why does the body need the heart to beat so fast? One important part of that answer may be oxidative stress.

What Is Oxidative Stress?

Your cells constantly produce reactive oxygen species as part of normal energy production, immune defense and cellular signaling. Your body also has antioxidant systems, including glutathione, superoxide dismutase, catalase and other enzymes, to keep those reactive molecules under control.

Oxidative stress occurs when the production of oxidants overwhelms the body’s ability to neutralize and repair the damage. That damage can affect:

• Cell membranes and fats
• Proteins and enzymes
• DNA and RNA
• Mitochondria
• Autonomic nerves
• The endothelial lining of the blood vessels

That last point matters enormously in POTS. The endothelium helps govern vascular tone, nitric oxide production, tissue perfusion, inflammation and the movement of fluid between the bloodstream and tissues. Standing successfully requires an immediate, coordinated vascular response. Damaged or dysfunctional blood vessels can make that response much harder.

The POTS–Oxidative Stress Connection

POTS is not one disease with one cause. It is a syndrome with several recognized patterns, including low blood volume, excessive venous pooling, small-fiber or autonomic neuropathy, hyperadrenergic activation, impaired vascular function and autoimmunity. More than one can exist in the same person. Oxidative stress may connect several of these pathways.

1. Oxidative stress can reduce nitric oxide

Nitric oxide tells blood vessels when and how to relax. Under oxidative stress, superoxide can react with nitric oxide to form peroxynitrite. This reduces the nitric oxide available for healthy vascular signaling while creating another reactive molecule capable of damaging proteins, membranes and mitochondria.

The result can become a vicious cycle: more oxidative stress leads to less available nitric oxide, worse endothelial function, impaired blood-flow regulation and greater physiological stress.

This is not merely a biochemical theory. A 2021 study found impaired flow-mediated dilation in the conduit arteries of people with POTS, supporting systemic endothelial dysfunction as part of the syndrome in at least some patients. Read the study here.

2. Antioxidant intervention changed circulation in human POTS

One of the most compelling studies examined 11 people with low-flow POTS and eight controls. Low-flow POTS was characterized by vasoconstriction, reduced cardiac output, increased angiotensin II, reduced bioavailable nitric oxide and oxidative stress. The researchers administered ascorbate, an antioxidant form of vitamin C, and measured blood flow and vascular responses.

In the POTS group:

• Nitric-oxide-dependent skin blood-flow responses improved.
• Cardiac index increased by approximately 40%.
• Peripheral resistance, which had been nearly twice that of controls, fell by almost 50%.
• Abnormal calf vascular measures moved toward normal.

The investigators concluded that the results provide experimental support for oxidative stress and reduced nitric oxide contributing to the abnormal vasoconstriction of low-flow POTS. Read the controlled clinical study.

3. Oxidative stress may impair blood flow to the brain

The usual POTS sensation is not vertigo, the rotary feeling that the room is spinning. It is more often lightheadedness, presyncope, dimming vision or brain fog. These symptoms can occur when upright cerebral blood flow is inadequate. Research has documented cerebral hypoperfusion in orthostatic intolerance, even in some patients without a major fall in blood pressure. Read the cerebral blood-flow study.

If the brain is not receiving adequate blood flow when you stand, the body may answer with tachycardia and a surge of stress hormones. Again, the fast heart rate may be compensation, not the original defect. We see the same pattern behind many of the causes of a high heart rate we investigate every day.

4. Inflammation, immunity and oxidative stress feed one another

Many cases of POTS begin after an infection, pregnancy, surgery, trauma, prolonged inactivity or another major biological stressor. Postviral onset is common, and immune-mediated mechanisms are being investigated in subsets of patients. Read the clinical review.

Immune activation generates oxidants as part of the body’s defense. Oxidative damage can then activate additional inflammatory pathways. If the cycle does not shut off, the original trigger may be gone while the biological aftermath continues. This connection may be especially relevant in post-infectious POTS and Long COVID-associated POTS, though that work is early and should not be generalized to all POTS.

5. Mitochondria and the autonomic nervous system are vulnerable

Mitochondria make the energy required for vascular contraction, nerve signaling, sodium-potassium balance and recovery from exertion. They are also a major source and target of reactive oxygen species.

When mitochondrial function falters, energy production can fall while oxidant production rises. Oxidative damage may then further impair the mitochondria. That loop offers a plausible connection among fatigue, exercise intolerance, poor recovery and autonomic instability, although it remains one component of a much larger and still-evolving POTS picture.

What May Be Driving the Oxidative Stress?

Finding oxidative stress is not the end of the investigation. It is the beginning of a better question: why is oxidative stress elevated in this person?

My root-cause framework is simple: too much bad stuff, not enough good stuff.

The bad stuff may include infections, water-damaged buildings, mold and microbial fragments, pesticides, plastics, heavy metals, ultra-processed foods, medications, poor sleep, artificial light at night, chronic stress and other environmental burdens.

The missing good stuff may include sunlight, darkness at night, restorative sleep, clean air and water, nutrient-dense food, minerals, movement appropriate to the person’s capacity, healthy relationships, nature and purpose.

These inputs can influence the gut, immune system, endothelium, mitochondria and autonomic nervous system. But no two people arrive at POTS by precisely the same route. One person may have oxidative damage driven primarily by chronic infection and immune activation. Another may have major toxicant exposure. Another may be nutrient depleted. Many people have several contributors at once. That is why a generic antioxidant protocol is still guessing.

Every Person With POTS Deserves a Deeper Investigation

I am not saying oxidative stress is the only cause of POTS, or that every person with POTS will have the same abnormal markers. The evidence does not support that claim.

I am saying oxidative stress is biologically relevant, linked to pathways already documented in POTS, and measurable. Anyone with POTS deserves to know whether it is part of their picture and what may be driving it.

Do not guess that you need more antioxidants. Do not guess that your blood vessels are healthy. Do not guess whether toxins, nutrient deficiencies, inflammation or metabolic dysfunction are a factor. Test, don’t guess.

Good, Better and Best: Choose Your Next Step

Good: Oxidative Stress Test

Start here if you want a focused, affordable look at oxidative damage. Our simple at-home urine test measures lipid peroxides, evidence that oxidative processes are damaging fats. It gives you objective information about a pathway that may affect endothelial function, nitric oxide signaling and circulation.

This is an excellent first step for someone asking: is oxidative stress showing up in my biology? Start with the Oxidative Stress Test.

Better: Cardio Zoomer

POTS is rarely about one pathway. The Cardio Zoomer provides a much broader blood-and-urine assessment of cardiovascular biology. It brings together markers of:

• Oxidative and redox stress
• Endothelial function and nitric-oxide biology
• Inflammation
• Metabolic health
• Advanced lipids, lipoproteins, ceramides and sterols
• Omega fatty-acid balance
• Cardiac stress and clotting
• Relevant genetic tendencies

This is the better choice when you want to ask how oxidative stress, inflammation, metabolism and vascular function are interacting in you. Go deeper with the Cardio Zoomer.

Best: 100 Year Heart Diagnostic Deep Dive

The best choice is for the person who wants to investigate not only the damage, but the potential drivers. The 100 Year Heart Diagnostic Deep Dive combines six advanced assessments:

• Cardio Zoomer
• Wheat Zoomer for gut permeability and immune reactivity
• Heavy Metals Test
• Mycotoxins Test
• Environmental Toxins Test
• Nutrient Zoomer for intracellular nutrient status

It also includes a personal review with a Natural Heart Doctor Master Health Coach, with an option to upgrade to a physician review. This is the best next step when you want to ask what is damaging your biology, what you are missing and where to focus first. Choose the 100 Year Heart Diagnostic Deep Dive.

The Diagnosis Is the Starting Line

POTS tells you what happens when you stand. It does not tell you why it happens.

Oxidative stress may damage the endothelium, reduce available nitric oxide, impair vascular regulation, disrupt mitochondrial energy production and amplify inflammation. Human studies show that these pathways are relevant in at least some people with POTS.

The next step is to determine what is true for you. Get the data. Identify the patterns. Look for the drivers. Then build a plan around your biology, not someone else’s assumptions. Good: measure oxidative damage. Better: map cardiovascular, endothelial and metabolic function. Best: investigate the broader network of oxidative stress, gut permeability, toxins and nutrient status.

If you have POTS, test, don’t guess. If you want help interpreting your own picture, schedule a discovery call with our team. You may also want to read our work on natural solutions to sinus tachycardia.

– Dr. Jack Wolfson, DO, Cardiologist and Founder of Natural Heart Doctor

Medical note: POTS requires appropriate clinical diagnosis and evaluation. New or severe chest pain, fainting, shortness of breath, neurological symptoms or marked tachycardia may require urgent medical assessment. These specialty tests do not diagnose POTS, identify a single proven cause or replace medical care; they provide additional data that should be interpreted in the context of symptoms, examination and standard diagnostic testing.

References

• Stewart JM, Ocon AJ, Medow MS. Ascorbate improves circulation in postural tachycardia syndrome. Am J Physiol Heart Circ Physiol. 2011;301(3):H1033-H1042. PubMed
• Chopoorian AH, et al. Impaired endothelial function in patients with postural tachycardia syndrome. Hypertens Res. 2021;44:657-664. Full text
• Del Pozzi AT, Schwartz CE, Tewari D, Medow MS, Stewart JM. Blunted cerebral blood flow velocity in response to a nitric oxide donor in postural tachycardia syndrome. Am J Physiol Heart Circ Physiol. 2014;307(3):H397-H404. PubMed
• Novak P. Hypocapnic cerebral hypoperfusion: a biomarker of orthostatic intolerance. PLoS One. 2018;13(9):e0204419. Full text
• Raj SR, et al. Diagnosis and management of postural orthostatic tachycardia syndrome. CMAJ. 2022;194(10):E378-E385. Full text

Frequently Asked Questions