Robert Groysman, MD

Robert Groysman, MD Physician with a focus on Long COVID, post-vaccine syndromes, ME/CFS, dysautonomia, POTS. Author of seven books on Long COVID. Early U.S.

clinical adopter of Epipharyngeal Abrasive Therapy (EAT). FB page not affiliated with practice.

06/14/2026

If your endoscopy came back clean, your celiac panel was negative, and you are still reacting to foods that never bothered you, the problem may not be the structure of your gut at all, but the chemical shield supposed to coat it.

The chemical shield is built from a few specific layers, and Long COVID can thin each one.

Secretory IgA. This is the antibody patrolling the mucosal surface of your gut, nose, and throat, catching invaders and irritants before they reach tissue. After COVID, IgA output commonly shifts. When it drops, the front line thins and more gets through.

The mucus layer. A physical coat over the gut lining, keeping bacteria at a distance from the cells underneath. Dysbiosis, the imbalance of gut bacteria, degrades this layer. The bugs meant to help maintain it are outnumbered.

The tight junctions. The seams between the cells of the gut wall, meant to stay closed so only fully processed nutrients pass. Inflammation loosens them, and partially broken food contents slip through into circulation, where the immune system meets them and responds.

Picture a fine kitchen sieve whose holes have widened. It was built to hold back everything but the water. Now the pasta goes through with it. The sieve is intact, the structure looks fine, but it is no longer doing the one job that mattered.

This is why a clean scope and a real food reaction are not a contradiction. The scope reads structure. The shield is chemistry, and chemistry does not show up on a picture.

Comprehensive stool testing can measure secretory IgA and map the bacterial balance underneath it.

(Consult with your doctor before starting any new treatment.)

06/14/2026

You woke up and something was different, lighter, the fog thinner than usual, and you lay still for a moment doing the thing you have learned to do, which is not to celebrate it but to test it, carefully, the way you would put weight on an ankle you were not sure about. You sat up slowly and the room held steady. No spike behind the eyes, no heaviness pooling in the legs, just a morning that felt almost like a morning used to feel, and immediately the question arrived, the only question that matters on a day like this, which is how much.

How much can you spend before the floor opens.

There is a version of you, the one from before, who would already be up and moving, treating a good morning as nothing remarkable because every morning was good. That version does not run the math. You run the math now whether you want to or not, weighing the laundry against the phone call, the shower against the errand, knowing that a good morning is not a promise and that the bill for guessing wrong does not come today, it comes tomorrow, or the day after, delayed and exact. So you sit on the edge of the bed in the unfamiliar quiet of feeling okay, and you do not trust it, not because you are pessimistic, but because trusting it is the most expensive thing you could do.

06/13/2026

A nervous system stuck in overdrive is not a permanent setting. It is a branch stripped of its counterweight, and the counterweight can be rebuilt.

In Long COVID dysautonomia, the sympathetic branch, the one speeding the heart and tightening the vessels and keeping the body braced, gets stuck on. The parasympathetic branch, the one meant to slow things down and signal safety, goes quiet. Most of this signaling travels the vagus nerve. When its tone drops, the brake stops answering and the body runs braced all day.

Vagal tone is not fixed at its lowest point. It responds to consistent, low-demand input over time, the same way an underused capacity slowly returns when it is asked for gently and often.

The first signs are quiet. Heart rate settling a little faster after you stand. A night where sleep goes a layer deeper. A meal leaving you neither wired nor crashed. A morning where the first hour is not a wall. None of these feel like recovery in the moment. They feel like ordinary days. That is exactly what they are supposed to feel like.

What helps the vagus is unglamorous and slow: paced breathing where the exhale runs longer than the inhale, gentle and consistent rather than intense, and genuine rest rather than the performed kind. The clinic also uses targeted approaches like the stellate ganglion block to help reset autonomic balance when the branch is stuck.

If you are braced and have been for months, the brake is not gone. It is quiet, and quiet can be brought back.

(Consult with your doctor before starting any new treatment.)

06/13/2026

Mast cells carry hundreds of chemical mediators, and histamine is only one of them.

This is why the antihistamine doing nothing for you was not proof your mast cells are fine. It may have been proof the mediator driving your flare was never histamine in the first place.

When a mast cell activates, it releases its load like an alarm system tripping every sensor at once. Histamine is the one everyone names. The others get missed.

Prostaglandin D2. This is the mediator behind the deep flushing, the drop in blood pressure, the aching arriving with a flare. Antihistamines do not touch it. It runs on a separate pathway, the same one certain anti-inflammatory medications act on.

Leukotrienes. These drive the airway tightening, the congestion, the wheeze feeling like asthma but not responding to an inhaler the way asthma should. A different class of medication targets these, and it is not an antihistamine.

Tryptase. Less a symptom-driver and more a marker. A blood level drawn at the right time can help confirm mast cells are activating, even when histamine looks normal.

The pattern this creates is a patient hitting symptom after symptom with the one tool they were handed, like a game of whack-a-mole where the mole keeps coming up in a hole the mallet cannot reach.

If a histamine-focused approach gave you partial relief or none, the result is information. It can point toward the non-histamine mediators and a workup needing to widen.

Bring this to a clinician who tests beyond histamine.

(Consult with your doctor before starting any new treatment.)

06/13/2026

You sat at the kitchen table after dinner and did the accounting the way you do every night now, quietly, before you let yourself think about tomorrow. You went through the day in order: the shower, the two hours of work, the call with your sister that ran forty minutes, the walk to the mailbox and back, the load of laundry you started and did not move to the dryer. Five entries. You ran the total against what you had started with, a number you cannot name or write down but that you know the way you know the weather before you check your phone, and you arrived at where you always arrive: less than you started with, more spent than you thought you spent, a small deficit that will have to come from somewhere. You closed the accounting the way you always close it, by deciding that tomorrow you would spend more carefully. Then you went and lay down, not because it was bedtime, but because lying down is the only way to stop paying interest on the day.

06/12/2026

The first 30 minutes after your thyroid medication decide how much of it your body actually uses.

Levothyroxine and other thyroid hormone replacements are absorbed in the small intestine. That absorption window is narrow and specific, and it is almost entirely spent before most patients get to breakfast.

What happens in those 30 minutes determines whether you received an effective dose or an expensive sip.

Take it on an empty stomach with a full glass of water. The tablet needs water to dissolve and an empty gut to reach the small intestine before food changes the pH and slows the uptake. Coffee does not count. Coffee interferes with levothyroxine absorption even black, enough to reduce uptake by roughly 20 to 36 percent in published studies.

Wait the full 30 to 60 minutes before eating or drinking anything other than water. The label says 30 minutes. For patients with gut dysbiosis or reduced motility, the window may need to be 60. If your levels have been erratic without a clear dose-change explanation, a longer pre-food window is worth trialing with your provider.

Keep calcium, iron, and magnesium separate. These minerals bind levothyroxine in the gut and carry it out before it absorbs. Morning supplements that contain any of these three should move to midday or evening. This includes calcium-containing antacids, which are easy to overlook.

Be consistent about timing, not just about taking it. Taking the dose at 7 AM one day and 9 AM another day shifts the spacing from the last dose and can create enough variation to show up as unstable TSH on labs. Same alarm, same time, every morning.

If you have recently started a probiotic, added a fiber supplement, or changed antacids, bring that to your prescriber alongside your next lab results. The absorption window is sensitive to changes that seem unrelated to thyroid function.

The medication is doing its part. The window is where the results are made or lost.

(Consult with your doctor before starting any new treatment.)

06/12/2026

Your body runs temperature regulation through one central thermostat and two response systems, and in Long COVID dysautonomia all three can misfire at the same time.

The thermostat is the hypothalamus, a small structure at the base of the brain, reading core temperature and dispatching signals telling the body to heat or cool. In a functioning autonomic nervous system, the signals arrive on time and the response follows: peripheral vessels dilate to push heat toward the skin for release, or constrict to keep warmth near the core; sweat glands activate to evaporate heat when needed.

When autonomic signaling is disrupted, the dispatch goes out but the response arrives late, distorted, or aimed at the wrong target.

Picture an elevator panel where the buttons still register a press, but sometimes it goes to a different floor. You press lobby. It goes to the second floor. The input is being received. The routing is the problem.

This is why patients describe a disconnect hard to explain to anyone who has not felt it. You step into a room you know is 68 degrees and your skin reads 85. You sit in the summer sun and stop sweating from the torso but your forehead runs freely. You spend a Long COVID morning sweating through a shirt in a cool house, then spend the afternoon unable to warm your hands in a heated car. The thermostat is reading something; the body is responding to something; the two are no longer reliably reading the same thing.

A second layer compounds this. Autonomic dysfunction can impair the sweat gland response itself. Sweating is a cholinergic response, meaning it depends on a specific branch of the autonomic nervous system. When that branch is underperforming, the body loses one of its primary cooling mechanisms even while the hypothalamus is calling for it.

The pattern this creates is not random. It has a signature. The misfires cluster around transitions: moving from sitting to standing, from inside to outside, from rest to light activity. Transition is when the autonomic system has to rapidly recalculate and dispatch, and in Long COVID dysautonomia, rapid recalculation is exactly where the system falls short.

Bring the pattern to a clinician testing autonomic function, not just thyroid or hormone panels. The signature points in a specific direction.

(Consult with your doctor before starting any new treatment.)

06/12/2026

Recovery from endothelial dysfunction almost never announces itself.

Patients do not notice it on a lab report. They notice it on the stairs.

One patient can describe it this way.

She had been climbing the same twelve steps for eight months, counting them every time. Three more. Two. One. She counted because knowing how many were left was how she managed the commitment, a calculation she ran without noticing she was running it, just to be sure the top would not arrive before she was ready for it. Then one afternoon she was talking, mid-sentence, and she reached the landing and finished the thought and only then noticed she had climbed without the count.

She did not tell anyone. It felt too small to say out loud and too large to risk saying wrong.

The next week it happened again, in the grocery store. She had taken to parking near the cart return so she could lean on the cart from the first step. She parked there out of habit and walked half an aisle before realizing the cart had been rolling two inches ahead of her, carrying nothing.

These are the moments I watch for. Not the dramatic ones. The quiet, provisional ones patients are almost afraid to trust, because they cannot tell yet whether they are the beginning of something or just a good Tuesday.

But this is how endothelial recovery tends to start. Microcirculation restores slowly, and the body reports the shift before the numbers catch up to it. The small capacities return first: the stairs climbed without counting, the cart you stop leaning on, the sentence finished on the way up.

If you are in the long middle of this and cannot feel any progress, watch the small moments. They are data too.

06/12/2026

Cetirizine, loratadine, diphenhydramine. The H1 antihistamines most Long COVID patients reach for first, and in MCAS they are covering less than half the receptor map.

Antihistamines are not wrong. The selection is incomplete.

Histamine binds to four receptor types. H1 and H2 carry most of the clinical load in MCAS. H1 receptors handle the familiar symptoms: runny nose, hives, itching, sneezing. The standard antihistamine targets this class.

H2 receptors sit in a different location. The stomach lining. The small intestine. The heart. They manage acid production, gut motility, and some cardiovascular signaling.

When mast cells release histamine in a Long COVID flare, they release into both receptor classes at once. The H1 blocker you took addresses the nose. The bloating, the heartburn, the palpitations keep going because those are H2 territory, and the H2 receptors received no coverage.

Famotidine and cimetidine are H2 blockers. Many MCAS patients find that adding H2 coverage alongside their H1 antihistamine, under a clinician's guidance, changes what had been partial relief into something that lands.

This is not a fringe approach. H1 and H2 blockade together is documented in the mast cell literature.

Ask your clinician specifically about H2 coverage if you are managing MCAS symptoms below the neck, the gut, the chest, the heart, and wondering why the antihistamine in your cabinet is not touching them.

(Consult with your doctor before starting any new treatment.)

06/11/2026

If you have ever felt the crash beginning, the heaviness settling into your legs, the words starting to slip out of reach, the familiar drop behind your eyes, and pressed on anyway because you were almost done, you know what the first ten minutes of a PEM crash can cost when you spend them wrong.

Those ten minutes are not just the opening of a bad day. They are where the length of the crash gets decided.

Post-exertional malaise is a mitochondrial energy debt called in faster than the cells can generate repayment. When output has exceeded what the energy system can sustain, the system does not slow down gradually. It drops. And in the first minutes after the drop begins, the cells are still attempting to run processes they no longer have the power to complete. Pushing through that window makes a withdrawal on an account that is already empty. Stopping early keeps the debt from compounding.

A protocol for the window:

Stop the activity the moment you recognize the signal. Not at a reasonable stopping point. Now. Every minute of continuation past the recognition point multiplies the cost, and the cost does not become visible until hours later.

Get horizontal. Sitting uses more energy than lying down. The body does less work maintaining posture; every unit of energy freed from posture is available for recovery. If lying down is not immediately possible, sit and stop all non-essential movement.

Remove demands on the nervous system. Dark if you can, quiet if you can, phone face-down. Input costs energy even when the body is still. This is not resting from your thoughts; it is reducing the total metabolic load while the cells begin to stabilize.

Stay there for longer than feels necessary. The temptation at ten or fifteen minutes is to check whether the crash has passed. Getting up to check is itself an output. Wait until the waiting feels easy rather than effortful. That shift in the quality of rest is the signal the system has begun to stabilize.

Cooling a crash does not mean it did not happen. It can mean the three-day version becomes a same-day version, and tomorrow does not get borrowed against.

(Consult with your doctor before starting any new treatment.)

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75093

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