Geoff’s Narration

The GIST

 

This blog is mostly about postural orthostatic tachycardia syndrome (POTS), but underneath it’s really about ME/CFS and long COVID. Why? Because a key factor in all four forms of POTS – and the other three other forms of orthostatic intolerance found in ME/CFS – are reduced blood flows, in particular, to the brain.

Whether the problem occurs in the brain or the muscles, the trigger for all these forms of orthostatic intolerance (problems standing) is a signal that the blood is not flowing properly. It’s not flowing properly for a number of different reasons, some of which we are still uncovering.

With POTS, ME/CFS, fibromyalgia, and long COVID, we seem to be looking a superstructure of diseases, all of which are characterized, in one way or another, by problems with blood flows.

This blog first takes a short look at POTS, then comes Geoff’s hyperadrenergic story (see the Zoom video), next a quick (pretty quick) overview of two recent hyperadrenergic POTS studies, and one possible new treatment.

Postural Orthostatic Tachycardia Syndrome (POTS)

“I think POTS is one of the greatest drivers of their illness. It’s vastly underrated and misunderstood… and until I fix or manage, I should say, their POTS, I can’t make progress… and I can’t deal with other things. I can’t treat their infection until I get their POTS down. If you as a patient say something about POTS and the doctor doesn’t know about it or doesn’t believe in it – you try to finish quickly and get out….there’s no point in continuing.” Dr. Kaufman

Postural orthostatic tachycardia syndrome (POTS) is turning out (like most diseases?) to have several flavors. Strictly speaking, POTS refers to a condition in which standing upright results in a sustained increase in heart rate of 30 beats per minute (bpm) in adults and 40 bpm in adolescents (ages 12-19).

If your symptoms flare while sitting or standing, you may have POTS or another form of orthostatic intolerance. You may experience symptoms such as lightheadedness, dizziness, palpitations, chest discomfort, shortness of breath, tremulousness (shakiness), generalized weakness, fatigue, and brain fog, which are relieved by their lying down.

The POTS Mimics – There are people who fit the tachycardia criteria but who do not experience symptoms when upright. They have high heart rates when upright but do not feel dizzy, etc., apparently because the blood flows to their brains are not affected. They do not have POTS.

Again, notice the emphasis on blood flows. Khan and colleagues recently published a review article, “Cerebral Blood Flow in Orthostatic Intolerance“, which asserted that reduced blood flows to the brain are the critical finding in all cases of (diagnosed) orthostatic intolerance and in people with ME/CFS who do not exhibit increased heart rates/altered blood pressure when standing.

Novak and Systrom recently assessed hundreds of people with ME/CFS and/or long COVID, the vast majority (88% / 92%) of whom showed reduced blood flows to the brain.

The heart rate and blood pressure issues in POTS, while real, are kind of a chimera. The main issue appears to be reduced blood flows to the brain, which can be produced in a variety of ways.

Hyperadrenergic POTS (HyperPOTS)

There are three types of POTS – and they can overlap. Check a description of them at the end of the blog. The two studies in this blog and the talk with Geoff concern one of the scariest type of POTS – hyperadrenergic POTS.

HyperPOTS is no laughing matter. The chronic symptoms are pretty standard: increased resting heart rate, feeling “wired but tired”, sensory sensitivity, and poor sleep. A hyperadrenergic attack, though, that’s something else.

Standing, exercise, large meals, heat, and even sensory stimuli can trigger an attack, which produces massive surges in catecholamines (norepinephrine) that cause the blood vessels to clamp down; the heart rate, the force of the heart’s contraction, and sometimes the blood pressure all to skyrocket.

A wide range of symptoms can occur, including palpitations, chest pressure, cold and sweaty hands and feet, physical tremors, internal shaking, intense panic/anxiety, light sensitivity, flushing, nausea, dizziness, and prolonged fatigue. They can, not surprisingly, send a hyperadrenergic POTS patient rushing to an emergency room.

They’re not having a heart attack. The autonomic nervous system centers in their brains have simply gone wild. HyperPOTS is caused by brain-induced surges in the levels of sympathetic nervous system-activating chemicals called catecholamines (mostly norepinephrine).

It’s not clear what percentage of people with POTS have hyperadrenergic POTS, but it’s believed to be about 24-40.

Two recent papers from Vanderbilt University – one of the top dysautonomia centers in the world – expanded our understanding of hyperadrenergic POTS and identified a new subtype.

But first, let’s hear from a hyperadrenergic POTS patient. Thanks to Geoff for being willing to share his story.

Geoff’s Hyperadrenergic POTS Story

You’ll see that my microphone cuts out from time to time. Figuring out what’s going on has been a challenge. If you see me looking away at times its because I’m looking something up on my computer.

 

As noted earlier, Geoff narrates “The Gist”. As I was emailing him, he temporarily disappeared a couple of times, only to reappear after an emergency visit.

His symptoms astounded me. Geoff tells his story best on our Zoom call, but the nuts and bolts are: Geoff was managing with ME/CFS, but when hyperadrenergic POTS showed up, that changed everything. Check out a few highlights below.

Step I: a Few Hints – Up until his mid-twenties, Geoff was pretty healthy. He had some hints (family history of hypercholesterolemia (high cholesterol levels), anemia, and profound fatigue) that something was off, but swimming (notice that it’s supine!) boosted his energy significantly.

Step 2: Cold Susceptibility – During his 20s, he noticed that he seemed to be particularly susceptible to colds and took longer to get over them – possibly a sign that his immune system either wasn’t up to snuff with pathogens and/or became hyperactivated when it encountered them.

Step 3: The Initial Trigger – During a 2003 internship at a permaculture center in the San Juan Islands, Washington state), he experienced dozens of tick bites. Not knowing about Lyme disease at the time, he just brushed them off, but within a year began experiencing severe, flu-like crashes during spring – just the time he was needed for gardening, landscaping, and teaching/consulting work.

Step 4: The Slow Build – Over the next ten years, things began to slowly devolve. He was still working but experiencing increased fatigue, flu-like symptoms, and pain.

Step 5: The Decline Accelerates – A car accident and a stressful job surely didn’t help, but his decline increased. He was still able to survive a work week, but then collapsed during the weekend. Then, though, he began having trouble making it through his work week at all.

Step 6: Disability – By around 2015–2016, he could no longer maintain regular employment and went on disability (PWD in BC). He greatly scaled back his permaculture nursery/teaching work but was able to keep a simplified food garden going. Diagnosing himself with ME/CFS, he applied and, after a 4-year wait, entered the BC Complex Chronic Diseases Program. While the program was validating, it did not provide much help.

Step 7: Partial Remission (!) – It’s unclear why, but during the spring and summer of 2020 he experienced enough of a partial remission to resume activity levels (cycling, kayaking, etc) that he had not been able to sustain in years.

Step 8: The Life-Altering Crash – Suddenly, in the fall of 2020, as access to in-person medical attention in BC became restricted in response to the pandemic, Geoff slipped into the biggest crash of his life. He experienced a severe and prolonged illness that Drs later confirmed was most likely shingles. He lost 25–30 lb, experienced tremors, “electrocuted” sensations, loss of appetite, and a strange scalp lesion. He also came down with hyperPOTS.

Geoff had been successfully using cannabis for years to help with his fibromyalgia pain, but suddenly his response to an edible form of the drug flipped: instead of pain relief, it started causing sensations of being “electrocuted” and caused his heart rate and blood pressure to spike to 170 bpm and 220/100. He made his first trip to the emergency room (and stopped using cannabis completely).

The Cannabis Surprise

Cannabis isn’t as benign as it seems. Unbeknownst to him, by using cannabis to help with his pain, Geoff was already stressing his sympathetic nervous system. For all its sedating and calming effects, the THC in inhaled or ingested cannabis activates the sympathetic nervous system.

Studies indicate that when inhaled, smoked, or vaped, large amounts of THC hit the brain rapidly. It has almost paradoxical effects on the autonomic nervous system. It raises the heart rate, causing a blood pressure surge, but then also dilates the blood vessels.

When ingested or taken orally, the situation is even more complicated. The THC from cannabis takes longer to hit (30-60 minutes), and when it does, the sympathetic nervous system (fight-or-flight) response may be blunted a bit, but it too can increase heart rate and alter blood pressure. (It sometimes lowers blood pressure, but if you also have hypovolemia (low blood volume), as many POTS patients do, that could cause an even greater heart rate surge).  In some chronic pain patients, it’s been shown to increase parasympathetic nervous system functioning and improve prefrontal cortex activity – two things we presumably want to see – but they don’t have hyperadrenergic POTS.

If you have the kind of twitchy autonomic nervous system found in hyperPOTS you’re essentially rolling the dice by using a cannabis product with THC. There’s basically no telling what’s going to happen. You’re affecting different parts of an already unbalanced autonomic nervous system with no clear outcome. Plus, if a hyperadrenergic POTS patient responds poorly to gummies, their longer-lasting effects may mean they are stuck for hours.

If you have hyperPOTS, it’s probably best to stay far, far away from THC.

Back to Geoff’s Story

Over time, Geoff developed repeated hyperadrenergic attacks during which his BP would bump up as high as ~246/110, and experience tachycardia, cold sweats, chest pain, “electric shocks”, and feelings of intense physiological panic. Between the surges, he had classic hyperadrenergic POTS physiology: standing, eating, or even doing dishes could dramatically raise his HR and BP.

This gardening/permaculture expert who’d been able to regularly engage in physical work, went from managing his illness (resting on weekends), to cutting down his work, and then abandoning it altogether, and now was having trouble standing and doing the dishes.

The CPAP Rescue

Then, Geoff caught a break. A sleep study found that he had sleep apnea, and using CPAP caused his hyperadrenergic attacks to completely stop for a year. His ME/CFS remained, but the emergency room stops were over. CPAP apparently worked because it reduces the sympathetic nervous system surges that accompany sleep apnea.

It’s Not Over Until it’s Over … and it’s Not Over

In the summer–fall of 2025, a period of chronic external stress appears to have gradually retriggered the hyperadrenergic attacks and ER visits. (Geoff added psychosocial stress to his list of hyperPOTS triggers.)

Hyperadrenergic POTS has caused him to radically prune his activities and stop his business/teaching work. At times, he’s had to have someone drive him in case an attack occurs. Thankfully, he’s been able to keep his garden, which provides him with organic food he couldn’t otherwise afford.

Repeated experiences of “I might die today” and his understanding of his need to get his flight/fight system under control have led him to embrace non-pharmacological ways to reduce the sympathetic nervous system activation, such as meditation and contemplative prayer. Practices that stabilize attention, emotion, and breathing have more leverage on his hPOTS than on ME. They don’t take care of it but hopefully make his system less prone to attacks.

He’s used AI to help understand his condition and assess treatment possibilities. He’s also developed ways to ameliorate the attacks when they come.

Managing the HyperPOTS Attacks

Geoff has found that his attacks follow a pattern.

First comes a diffuse, visceral sense that something is wrong. Next, he feels chest pressure (no increases in blood pressure or heart rate have occurred yet). He begins to shake, feels cold, and will need extra clothing or blankets to warm up. Next, blood pressure and heart rates may spike. Anxiety and feelings of panic can occur.

Geoff has found several things that can help when the attacks come:

(A) When he can feel his system is starting to surge, he lies on his left side doing deep breathing exercises and does self-calming techniques.

(B) If that’s not enough, then 0.5 mg sublingual Ativan (lorazepam) can help. Ativan doesn’t affect the brain surges of norepinephrine, but it can calm the body down.

(C) Clonidine – If that’s not enough, he goes to the nuclear option – clonidine -which can bring his blood pressure down within an hour or so (and prevent an ER visit). (It can also trigger a rebound effect later. Ironically, he learned about clonidine from a doctor during an ER visit. Usually, half the described dose is enough. He had been using metoprolol, but it was lowering his heart rate but spiking his blood pressure.)

(D) Gabapentin (100 mg doses staggered every 1–2 hours (e.g., 3–4 doses) can be surprisingly helpful. They can also help at night (100 mg at 9, 10, and 11 pm) to prevent nighttime surges and improve sleep quality. On his worst PEM days, a daytime 100 mg dose can “take the edge off” the flu‑like crash and pain.

He’s aware of guanfacine but has not started it because only extended‑release is available to him, making titration and tapering harder and adding cost.

The Studies

Will the Real Hyperadrenergic POTS Stand Up?

Now to the “Hyperadrenergic Postural Tachycardia Syndrome: Clinical Biomarkers and Response to Guanfacine” study. Despite the fact that hypadrenergic POTS appears to be common in POTS, it doesn’t get much study. Two recent studies, however, have been published. The first clarified how to determine who has hyperPOTS and validated a treatment. The second opened up a whole new kind of hyperPOTS.

The current diagnostic guidelines for hyperadrenergic POTS require upright norepinephrine levels of ≥600 pg/mL and/or paradoxical upright increases in blood pressure.

These researchers questioned whether these criteria are accurate enough. They noted that people with other types of POTS, such as hypovolemic POTS and neuropathic POTS, can meet the criteria for hyperadrenergic POTS. The POTS produced in these patients results from compensatory reactions to low blood volume and/or nerve damage in the lower body – not from a brain-based surge in norepinephrine.

It’s important to get the diagnosis right because the treatments for each type can be quite different and even contraindicated.

The confusion arises because researchers and doctors are measuring norepinephrine (NE) levels in the blood, which is produced by the peripheral nerves (nerves in the body), and NE levels tend to be high in all these types of POTS.

The question is, did the NE spike occur because a setpoint in the brain is off (hyperadrenergic POTS), or because of low blood volume (hypovolemic POTS), and/or because of nerve damage (neuropathic POTS)?

The authors used the Valsalva maneuver to stress test the autonomic nervous system while assessing things like muscle sympathetic nervous system (MSNA), supine/upright plasma norepinephrine, and BP responses.

The Valsalva Maneuver

In the Valsalva maneuver, which was created by the Italian anatomist Antonio Maria Valsalva in the early 1700s (!), a patient blows into a mouthpiece to maintain continuous pressure for 15 seconds. A healthy nervous system produces four predictable phases.

Blowing hard compresses the aorta, preventing blood from returning to the heart and causing the amount of blood leaving the heart to plummet. First, the blood pressure spikes, and then the brainstem, alarmed at the reduction in blood flows, dumps norepinephrine into the bloodstream to constrict the blood vessels and raise the heart rate in an attempt to get the blood flowing again.

When the patient stops blowing, the blood suddenly floods back into the heart, and the crucial moment comes. Blood pressure drops, but the heart, now filled with blood, slams the blood into the still-constricted blood vessels, sending the pressure shooting up again. The brain immediately activates the vagus nerve, sending parasympathetic activity soaring to bring the heart rate and blood pressure down.

In hyperadrenergic POTS, everything is off kilter. The drop in pressure during the first part of the test triggers an immediate, massive flood of norepinephrine, which spikes blood pressure and heart rate and constricts blood vessels into tiny tubes.

When the participant stops blowing on the tube, and their heart starts pumping again, it’s now pumping blood into small blood vessels that have been slammed shut by all the norepinephrine.

That’s too much for the parasympathetic nervous system to handle, resulting in an exaggerated and prolonged diastolic blood pressure surge. It’s this blood pressure surge that the researchers used to determine if someone had hyperPOTS.

Finally – the REAL Hyperadrenergic POTS (hyperPOTS) Patients

Because in hyperadrenergic POTS, norepinephrine levels are always high, but in hypovolemic and neuropathic POTS, they are only high upon standing, the authors assessed muscle sympathetic nervous system activity while the patients were lying down to determine who had hyperPOTS. They also used levels of a factor called ΔDBP_VM2, which is tightly linked to brain sympathetic nervous system activity, to determine which POTS patients actually had hyperadrenergic POTS.

They found that an increase in DBP >17 mm Hg during phase 2 of the Valsalva maneuver to be a useful clinical biomarker of hyperPOTS. Now they had a more accurate diagnostic test for hyperadrenergic POTS than NE levels.

The Guanfacine Gambit

Then, they took a group of POTS patients, and using their new Valsalva maneuver measures, differentiated them into POTS and hyperPOTS patients and gave both sets of patients guanfacine, a drug that is able to tamp down brain-induced surges of norepinephrine.

While both sets of patients took guanfacine, only the true hyperPOTS patients benefited from it. Symptom severity, attack frequency, impact on daily activities, and fatigue all dropped. People without hyperadrenergic POTS improved less or not at all.

The end result – a more accurate test for hyperadrenergic POTS and a drug that helps.

Note that a small study found that guanfacine plus NAC improved cognition in long COVID.

The Blood Vessel Hyperadrenergic POTS Subset Shows Up

Now that they were able to more accurately identify hyperPOTS patients, they dug deeper and uncovered a new hyperPOTS subset. The study, “Hyperadrenergic postural tachycardia syndrome associated with augmented neurovascular transduction“, once again, used the Valsalva maneuver to stress test the autonomic nervous system.

This time they used a technique called peripheral sympathetic neurovascular transduction, or psNVT, which measures the extent to which blood pressure changes in response to sympathetic nervous system activation. They found an anomaly in a significant subset of hyperPOTS patients during late phase 2 of the maneuver.

It involved blood pressure. The authors expected that hyperPOTS patients with the greatest increases in blood pressure would also exhibit increased sympathetic nervous system activation. They did not. They had the same sympathetic nervous system activation but a greatly enhanced response in their blood vessels. Instead, their blood vessels appeared hyper-responsive to norepinephrine.

Note that this bigger blood pressure spike isn’t just about blood pressure, per se. That blood pressure spike may make it more difficult for blood to get to the brain, muscles, gut, etc., causing more problems with orthostatic intolerance, exercise intolerance, brain fog, and PEM. Plus, because the hyperPOTS blood flow problems originate in the brain, people with hyperPOTS may have more difficulty regulating blood flows in the brain.

So now we have another type of hyperPOTS – one that is associated with overly twitchy blood vessels. (One way or another, it always seems to come back to blood flows.)

Causes

Now to the nitty-gritty. What could be causing twitchy nerves in the blood vessels of hyperPOTS patients to overreact to norepinephrine? As usual, it’s possible that a bunch of things could. Note, though, that none of these are beyond our capacity to assess – and most of them are already being assessed in ME/CFS and long COVID.

That makes it possible that a breakthrough in ME/CFS/long COVID could produce a breakthrough in hyperPOTS, and vice versa. All forms of POTS, after all, seem to exist as a compensatory response to problems with blood flows (see the forms of POTS below).

Receptor issues – The receptors that react to norepinephrine (adrenergic receptors) may be too touchy or there may be too many of them (more receptors = a quicker response).

This is an interesting option for the ME/CFS field, as a subset of ME/CFS patients clearly appear to have altered adrenergic/muscarinic receptor activity. If the B2 adrenergic receptors, in particular, don’t dilate the blood vessels enough, the blood vessels will be too narrowed. That would cause (see endothelial cell dysfunction below) the blood vessels to over-respond to the same amount of norepinephrine.

This seems very similar at first glance to Wirth/Scheibenbogen’s thesis that vasodilators are flooding the area in an attempt to open closed blood vessels.

Reduced reuptake – Too much norepinephrine lingering in the nerve synapse (most of it is usually taken back up quickly) could result in prolonged vasoconstriction and an extra hit during a hyperadrenergic attack.

Endothelial cell dysfunction – reduced nitric oxide levels would also prevent the blood vessels from dilating normally. If the blood vessels are already shut down, any further signal to constrict them more would simply get amplified. There’s ample and growing evidence that endothelial cell dysfunction is present in fibromyalgia, ME/CFS, and long COVID.

Mast cell activation – Mast cell activation is a prime candidate because mast cells can alter how responsive the receptors are (see option 1) and impair endothelial cell functioning (option 3). Mast cell activation, of course, is a candidate in a lot of things, including connective tissue problems in all these diseases. We desperately need better mast cell activation tests and treatments.

Blood vessel remodeling – recent blogs have touched on some evidence that that blood vessels may have become remodeled; i.e stiffened and less responsive. If the blood vessels are less pliable and responsive, the same amount of sympathetic nervous system signal would result in increased blood pressure.

We’re still missing something. Yes, all these things could trigger the sympathetic nervous system in the brain to react, but why the tremendous overreaction? An adrenergic surge triggered simply by standing or sitting up can, after all, send a person to their knees and land them in the emergency room. There must be something going on in the brain to produce this.

On the face of it, the twitchy hyperadrenergic POTS brain seems very much like the hypersensitive, hyper-responsive responses in pain in fibromyalgia, and the overreactions to chemicals/drugs/exertion in ME/CFS and long COVID.

The bad news is that a number of potential causes exist. The good news is the same – we have ideas what’s causing this – we just need to get after them.

• Genetic Mutations – an A457P mutation in the SLC6A2 gene found in two family members with POTS was shown to cause the NET transporter that removes NE from the nerve synapse to almost completely fail. This causes NE to build up and stay built up, leading to NE surges. Subsequent very small studies failed to find the mutation again. The finding did, however, lead to another possibility.
• Epigenetic Changes – a small 2012 study (n=16), however, suggested that epigenetic changes may cause the NET transporter to fail in many more POTS patients. Another study found that temporarily knocking out the NET transporter actually produces POTS in healthy people. Clear evidence from three different sources points to NET transporter dysfunction, but there the saga ends. No followup studies have been done.
• Autoimmunity – a few studies suggest that autoimmune antibodies that are attacking the adrenergic receptors are in play, but this hypothesis, a popular one, is still in flux.
• Mast cell activation – again, because mast cells cluster around the autonomic nerves, mast cell activation could be tweaking them.
• Hyperactive blood vessels – in some patients, abnormally acting blood vessels may be reacting too strongly to NE levels.
• Reduced blood flows to the brainstem – reduced blood flows to the primary regulator of the sympathetic nervous system found in the brainstem (the locus coeruleus) could be causing it to act up and pump out norepinephrine.

Notice that every possible cause but one is being actively investigated in ME/CFS and long COVID. These fields keep revolving around each other, which is why we need dedicated research programs that explore them all at once.

Treatment

The authors suggested that a drug called moxonidine might be helpful. Like guanfacine and clonidine, moxonidine can reduce sympathetic outflow in the brain. It’s available in some European countries and Canada but is not FDA-approved in the United States.

If both guanfacine and clonidine reduce sympathetic nervous system activity in the brain, why turn to a drug that isn’t currently available in the U.S.? Because moxonidine may be much more effective.

At first glance, moxonidine seems like an odd choice. The hyperactive blood vessel hyperPOTS subset doesn’t, after all, have increased sympathetic activity in the brain compared to the normal blood vessel hyperPOTS group.

So why target brain SNS activity rather than the blood vessels in the periphery or elsewhere in the body? Because reducing brain SNS activity could help reduce the blood vessel over-reaction. Increased brain SNS activity can also cause reductions in blood volume – a common finding in hyperPOTS, and drugs that tamp brain SNS activity could boost it.

Guanfacine turns down sympathetic nervous system activity by mimicking norepinephrine and tricking the adrenergic receptors it binds to into believing that too much NE is present. The receptors it binds to come before the nerve synapse.

It also binds to and activates adrenergic smooth muscles lining the blood vessels. Here’s where it gets tricky. The receptors it binds to in the blood vessels come after the nerve synapse. Instead of shutting down SNS activity, guanfacine actually amps it up in the body’s blood vessels, potentially further vasoconstricting them.

In normal hyperPOTS, the reduction in SNS activity in the brain far outweighs any minor vasoconstricting activity that may go on in the blood vessels of the body. The blood vessels in the twitchy blood vessel hyperPOTS subset are already hyperactive, though. They don’t need to be shut down further.

It’s not that guanfacine is bad for hyperPOTS patients. On the contrary, the small studies done so far suggest it’s helpful, but another drug that purely targets the brain might be more helpful, and that’s where moxonidine comes in.

Moxonidine also targets a different receptor (the Imidazoline-1 receptor) that turns down sympathetic nervous system activity in the brainstem. It also causes less dry mouth, sedation, and cognitive fatigue than guanfacine or clonidine.

Clonidine is an Imidazoline-1 receptor agonist, but it also affects alpha-adrenergic 2A receptors, so it can produce a similar problem. Rilmenidine is another pure imidazoline-1 receptor agonist which is available in Europe but not in the U.S.

These researchers tested moxonidine in a small group of “blood vessel” hyperPOTS patients, and it helped. Several measures taken during the Valsalva test (baseline SBP, decreased SBP overshoot, prolonged PRT, and most importantly, lower DBPVMNe) improved.

• An upcoming blog takes on the 7 (8?) types of orthostatic intolerance found in ME/CFS, fibromyalgia, and long COVID

Health Rising’s Quickie Donation Drive Update

Thanks to everyone who quickly brought us to over 15% of our goal. This blog presents a dilemma and an opportunity that is consistently showing up.

This blog took a while to write because it kept growing and growing. As I’ve been asserting, the connections just seem to keep piling up. You pull on one string and three more pop up!

Finally, I decided it was just too long, and it’s going to be broken into two more blogs – one on the rather remarkable growth of types of orthostatic intolerance (problems that accelerate while upright) that have been uncovered, and another that looks at the critical area of funding for ME/CFS, POTS, and long COVID at the NIH.

That’s just how things blow here. Deeper dives than usual are why Health Rising got started in the first place. If that floats your boat, please float ours with the amount of support that works for you 🙂

 

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