The autoimmune link between postural orthostatic tachycardia syndrome (POTS) and thyroid dysfunction is a complex puzzle. Symptoms of POTS and thyroid dysfunction can overlap, and clues that point to their root causes are frequently overlooked by physicians when treating patients. 

From my own personal experience with both conditions, to the countless stories shared by members of our community, we’ve seen a clear pattern where people struggling with POTS often learn they have thyroid dysfunction as well. The question then becomes, which came first? What’s the connection? And what does treating POTS with co-occurring thyroid dysfunction involve? 

This article isn’t meant to serve as exhaustive medical advice, but rather an examination of personal stories and public trends to reverse-engineer the autoimmune link between POTS and hypothyroidism. 

The Autoimmune Link Between POTS and Thyroid: A Case for Reverse-Engineering 

My diagnosis path was a classic case of addressing symptoms without finding their root cause. I was diagnosed with secondary POTS and told to drastically increase my sodium intake. I later learned the dangers of consuming excess iodine as my spinal-leak-caused food sensitivities (often mislabeled as Mast Cell Activation Syndrome (MCAS) by other patients on social media and even by physicians who attempted to push this diagnosis on me to create a zebra from a horse). 

I started eating eggs from hens fed enriched feed to increase my Vitamin D, B12, and Omega 3 intake due to my inability to eat meat. At the time, I had no idea what would unfold due to eating a high-iodine diet from many eggs per day, with the iodine content in each egg being 60 mcg. I have seen iodine intake increase as a common trend as individuals with secondary POTS. They change their diets due to food sensitivities, such as losing the ability to eat red meat and eating vast quantities of seafood and then note the onset of hypothyroidism. They also increase their sodium intake with table salt, not realizing that significant amounts of iodized table salt can be harmful. 

Little did I know at the time that I would find myself staring at a lab report a few months later that showed markers for hypothyroidism when I had never had thyroid issues before. We later ascertained that this hypothyroidism onset was because of my increased iodine consumption from the enriched eggs, alongside my improved Vitamin D and B12 levels and my improved cholesterol from higher Omega-3 intake.

This personal “aha!” moment sparked the idea of collecting patient stories and working backwards to identify trends. We examined the timelines, what changed, what was introduced, and what followed to find potential causal links that deserve a deeper look. 

That being said, correlation does not equal causation. Just because two conditions often appear together doesn’t mean one directly causes the other. However, these associations are vital cues in our reverse-engineering process. 

Connecting the Dots: EDS, Spinal Leaks, and Secondary POTS

One of the most telling clues we discovered while working patient stories backward is the role of the Ehlers-Danlos Syndromes. The EDSs are a category of connective tissue disorders that are often comorbid with POTS and autoimmune disorders. EDS is frequently associated with herniated disks, with some types creating more for specific spine issues. Small thoracic disc herniations are less common than cervical and lumbar herniations, but these herniations in the thoracic area–especially when calcified–are a major risk factor for spontaneous spinal CSF leaks. 

• The leak effect: A cerebrospinal fluid (CSF) leak can cause secondary autonomic dysfunction, which often looks identical to POTS. The body struggles to regulate heart rate and blood pressure. 
• The reversal clue: POTS caused by a CSF leak can be reversed by administering epidural blood patches. 

The Iodine Puzzle: Diet, Salt, and Thyroid Inflammation

Now, let’s circle back to that first piece of POTS advice my cardiologist gave me: increase your salt consumption. I did so, and thankfully, with kosher salt. Other patients have reported to us that they commonly use high amounts of table salt, averaging over 1,000 mcg of iodine a day, nearly reaching the upper limit, with research already showing that amounts of just 250 mcg/day in iodine supplements in sensitive populations were enough to show a significant tendency in provoking the onset of hypothyroidism, and sometimes hyperthyroidism. 

Research performed over decades suggests high iodine intake can be a double-edged sword.

The body needs iodine to produce thyroid hormones, but it must be in the right amounts since iodine has a U-curve of benefit. Too little is bad for the body, and too much can be just as harmful. For example, excessive iodine consumption can trigger or worsen autoimmune thyroiditis, like Hashimoto’s disease.

There’s an ongoing chicken-or-egg debate in medical research and public health spaces. Does high iodine consumption cause the autoimmunity, or does an underlying autoimmune tendency make people hypersensitive to normal iodine consumption? 

• The public health clue: Studies, like a large-scale population health Chinese study by Teng et al. (2006), have linked more-than-adequate iodized salt consumption (i.e., not even what is considered excess or toxic amounts) with an increased risk of autoimmune thyroid conditions, along with hypothyroidism with or without autoimmune thyroiditis.
• The modern finding: Recent research reveals that excess iodine intake creates inflammatory markers in other systems beyond the endocrine system, like the cardiovascular system. 

You may have started eating high amounts of iodized salt for POTS and later developed thyroid issues. There might be a familiar pattern of POTS onset followed by the sudden appearance of Hashimoto’s and/or hypothyroidism. It’s crucial to discuss this potential sequence of events with your medical team, as I learned personally that reducing iodine steadily led to easy reversal of hypothyroidism after a year of being hypothyroid. 

This was at the beginning of my thyroid journey, before I re-introduced iodine under the guidance of my medical team and ended up swinging hyperthyroid. Tracking changes in your iodine intake alongside changes in your thyroid panel and autoimmune markers can provide valuable data to potentially improve conditions and reduce the severity of your symptoms. 

Actionable Clues for Your Health Journey

So what should you do with all these interconnected clues? Tracking clues empowers you to be an active participant in your own recovery journey. Some steps to take include:

• Map out your health history: When did your POTS symptoms start? Did you increase your salt consumption? If so, what type of salt have you been consuming? When were your thyroid levels first checked? When were any changes noted? You’ll eventually start to notice patterns. 
• Investigate sources of iodine: Examine your diet closely. Are you using iodized salt liberally? Do you consume lots of seaweed, dairy, fortified or enriched foods, or certain supplements? Such foods are rich in iodine. Discuss your iodine intake with a doctor or dietitian.
• Consider the full picture: Bring up the possibility of EDS or related connective tissue disorder with your medical team if you have symptoms like joint hypermobility, stretchy skin, or easy bruising alongside POTS. Also consider whether your POTS is secondary. If your POTS is secondary to a spinal leak, you may have changes in your pituitary as a common brain MRI sign for spinal leaks, and these pituitary changes can have a direct impact on thyroid function as part of the hypothalamic-pituitary-thyroid (HPT) axis.
• Self-advocate with data: Walk into your appointment with a hypothesis that you would like tested. For example, you can say, "I have POTS and have been on a high iodized salt diet for a year. My fatigue, low appetite, and scary bradycardia (low heart rate) episodes started after I began high-sodium intake. These symptoms align with the sudden onset of an autoimmune thyroiditis and hypothyroidism diagnosis. I would like to explore whether my iodine intake is affecting my thyroid autoimmunity markers and hypothyroidism. Can we work with a dietitian in tandem to plan a gradual reduction of my iodine intake as I replace the table salt gradually with kosher salt and track my thyroid labs regularly, potentially monthly?” (Note that most US physicians are unlikely to know how to approach a plan for testing using the scientific method, so it can be helpful to create a plan yourself while researching and checking the literature, and then looping in your physicians and dietitians. If your physicians say “no,” ask them to note in your medical records that they refused. If they give strange advice or make comments that iodine does not affect the thyroid, ask them to provide sources to back up their claims and/or provide their rationale. Always balance assertiveness with a risk-benefit analysis in potentially being abandoned as a patient. As many US patients know, physicians are often quick to fire patients for asking questions or being too knowledgeable in areas where the physicians have low competence and low troubleshooting capability. You may need to introduce the idea more subtly to not create an ego threat to the physicians, which could result in you losing care.)

Your Next Step: From Clues to Strategy

Watch our course, Are You Consuming Too Much Iodine? Excess Intake & Thyroid Disorders, to untangle the complex web that connects changes in diet (including accidentally consuming too much iodine) due to food sensitivities and the onset of thyroid conditions. It will give you a structured starting point to evaluate what you’re eating and how it might be interacting with the different systems in your body. We’ll help you organize the clues so you can start having productive conversations. 

Sign up for our newsletter to get more stories, research breakdowns, and reverse-engineering frameworks delivered to your inbox. Join a community that thinks differently about chronic health puzzles. 

Let’s transition from being patients to detectives, and from detectives to advocates. The clues are there. It’s time to connect them and improve your quality of life. 

Disclaimer: This article is based on personal narratives and collected patient experiences interpreted through public health research. It is for informational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.