Robert Groysman, MD

03/13/2026

03/13/2026

Parasites: The Diagnosis That Gets Blamed for Everything

In many functional medicine discussions, parasites are often suggested as the hidden cause of fatigue, brain fog, gut problems, skin issues, insomnia, and dozens of other symptoms. The idea sounds plausible. Parasites exist. Some are common. But the reality in the United States is more nuanced.

Parasites absolutely do occur in the U.S. The most common ones include Giardia, Cryptosporidium, Enterobius (pinworms), and Toxoplasma. These infections usually have recognizable patterns. Giardia and Cryptosporidium typically cause diarrhea, bloating, and abdominal cramps after exposure to contaminated water, travel, daycare settings, or outdoor water sources. Pinworms are most common in children and cause nighttime a**l itching. Toxoplasma exposure is common but rarely causes symptoms in healthy adults.

When parasites cause illness, the clinical picture usually points in that direction.

What parasites usually do not do is cause years of unexplained fatigue, brain fog, anxiety, dizziness, dysautonomia, insomnia, or multi-system symptoms without clear gastrointestinal signs or exposure history.

Another issue is testing. Many “parasite panels” used outside standard labs are not validated the same way hospital or reference lab tests are. Some rely on stool microscopy from specialty labs that report organisms of questionable clinical relevance or detect harmless colonizers that live in many healthy people. This can make normal findings look like disease.

There is also a psychological component. When people have unexplained symptoms, they understandably want a concrete explanation. Parasites feel like something tangible that can be “cleansed” or eliminated. Unfortunately, in many cases the real issue lies elsewhere.

In conditions like Long COVID, ME/CFS, and dysautonomia, symptoms often come from dysfunction in systems such as autonomic regulation, mitochondrial energy production, endothelial function, immune signaling, hormone balance, or gut microbiome disruption. These mechanisms can produce symptoms that are very real, but they do not show up on a simple infection test.

Another point that is often misunderstood involves toxoplasma, a parasite many people worry about. Roughly 30–40% of adults in the U.S. have been exposed to toxoplasma, usually from undercooked meat or environmental exposure. In healthy individuals, the immune system quickly controls the infection and the parasite becomes dormant in tissue cysts. Most people never know they had it.

Even patients with Long COVID are still considered immunocompetent from an infectious disease standpoint. Long COVID can involve immune dysregulation, but it does not typically produce the type of severe immunosuppression seen in conditions like advanced HIV, chemotherapy, or organ transplantation. Those are the situations where toxoplasma can reactivate and cause serious illness. For the vast majority of people, dormant toxoplasma does not explain chronic multisystem symptoms.

That does not mean parasites should never be considered. They absolutely should be evaluated when the history makes sense.

Situations where parasite testing does make sense include:

• Recent international travel
• Exposure to contaminated water (lakes, streams, untreated water)
• Persistent diarrhea, especially with weight loss
• Household outbreaks
• Immunocompromised patients
• Eosinophilia on blood tests
• Specific exposure risks such as undercooked meat or animal contact

Outside of those contexts, parasites are usually far down the diagnostic list.

Medicine works best when diagnoses are guided by patterns, exposure history, and validated testing, not by whichever explanation is trending online.

Sometimes the most important step in solving chronic illness is not chasing the most popular diagnosis, but asking a different question:

Which biological systems could realistically explain the symptoms we are seeing?

03/13/2026

Comment I often see:
“Can we just call Long COVID what it is? It’s POTS like 80% of the time.”

It’s true that POTS and other forms of dysautonomia are very common in Long COVID. Many studies have shown that a large percentage of patients develop orthostatic intolerance, elevated heart rate when standing, temperature intolerance, brain fog, and fatigue. For some people, POTS is clearly the dominant problem.

But Long COVID is not the same thing as POTS.

Long COVID is a multisystem condition, and dysautonomia is only one of several major mechanisms that can be involved.

In clinical practice and research, we commonly see several overlapping biological drivers, including:

• Dysautonomia (including POTS)
• Mitochondrial dysfunction and energy impairment
• Endothelial dysfunction and microvascular issues
• Histamine excess or mast cell activation
• Gut dysbiosis and intestinal permeability
• Hormone dysregulation

Many patients actually have more than one of these mechanisms at the same time.

This is why two people with Long COVID can look completely different. One patient may have classic POTS symptoms, while another may have severe fatigue driven primarily by mitochondrial dysfunction, and another may have inflammatory or mast-cell related symptoms.

Another important point is that treating POTS alone does not always solve the problem. Some patients improve dramatically with POTS treatments, while others only partially improve because other mechanisms are still active.

So dysautonomia is very important in Long COVID, but reducing the entire condition to just POTS risks missing other treatable contributors.

Long COVID is better understood as a network disorder involving multiple interacting systems, rather than a single diagnosis.

Understanding which mechanisms are dominant in each patient is often the key to finding treatments that actually help.

03/13/2026

Is the MRI Usually Normal in Dysautonomia?

One of the most confusing things for patients with dysautonomia is that their MRI often comes back “normal.”

This leads many people to assume nothing is wrong. But that conclusion is often incorrect.

In most cases of dysautonomia, the problem is functional rather than structural. The autonomic nervous system is not regulating heart rate, blood pressure, vascular tone, and blood flow properly. Routine imaging of the brain or cervical spine frequently appears normal because standard MRI is designed to detect structural damage, not autonomic dysfunction.

Common mechanisms that cause dysautonomia but do not appear on MRI include:

• Autonomic nerve dysfunction
• Small fiber neuropathy
• Hyperadrenergic states
• Blood volume dysregulation
• Abnormal vascular tone
• Mitochondrial dysfunction
• Neuroinflammation

Because of this, many patients are told their MRI is clean even though their symptoms are severe.

However, there is another important nuance.

Some patients with dysautonomia do have cervical spine involvement, particularly in certain groups.

Situations where cervical issues may contribute include:

• Hypermobile Ehlers-Danlos syndrome
• Craniocervical instability
• Chiari malformation
• Cervical stenosis or disc disease
• Prior neck trauma (including car accidents)

The key problem is that routine MRIs are done lying flat and in a neutral position.

If symptoms are caused by dynamic compression or instability, the imaging may still appear normal. In some cases, abnormalities are only visible with:

• Upright MRI
• Flexion–extension MRI
• Dynamic imaging

This does not mean most dysautonomia is caused by cervical spine problems.

But it does mean that a normal MRI does not automatically rule out a cervical contributor in the right clinical context.

Clues that the cervical spine may be involved include:

• Severe neck pain or pressure at the base of the skull
• Headaches triggered by neck movement
• Symptoms worsening with certain head positions
• Arm numbness or weakness
• Balance problems
• Hypermobile joints or known Ehlers-Danlos syndrome
• History of neck trauma

The key takeaway:

A normal MRI does not rule out dysautonomia, and it also does not completely rule out cervical involvement when symptoms strongly suggest it.

Good medicine is about matching symptoms to the right mechanism, not just relying on a single test result.

03/13/2026

Your joints never ached before COVID. No family history of autoimmune disease.

Now you have elevated inflammatory markers, joint pain moving from one location to another.

I see this pattern in patients with post-COVID joint symptoms.

SARS-CoV-2 proteins share structural similarities with proteins found in human tissue. When the immune system generates antibodies against the virus during acute infection, some of those antibodies cross-react with the body's own proteins. This process is called molecular mimicry. The immune system cannot distinguish the viral antigen from the host protein it resembles. Autoantibodies targeting joints, nerves, blood vessels, or thyroid tissue are a direct consequence.

This is not classical autoimmune disease developing over years. It is an antibody response to a viral infection that misdirects itself against host tissue. The distinction matters for diagnosis because the titer levels are often lower than in established autoimmune disease, the multi-system involvement is unusual, and standard rheumatological panels may not capture the specific autoantibodies involved.

Testing to identify this pattern includes ANA panel, anti-phospholipid antibodies, complement levels (C3, C4), and inflammatory markers showing persistent systemic activation.

If joint symptoms, neurological symptoms, or multi-system inflammation appeared after COVID with no prior autoimmune history, autoantibody testing may identify the mechanism standard workups are missing.

Volume 1 of The Complete Long COVID Handbook covers immune dysregulation, molecular mimicry, autoantibody formation, and the diagnostic pathway for immune-mediated presentations after COVID.

03/13/2026

New floaters. Blurry vision that comes and goes. Light sensitivity making screens unbearable.

The standard eye exam evaluates structural integrity. Cornea, lens, retina, optic nerve, intraocular pressure. When all of these check out, the conclusion is nothing is wrong. But visual symptoms persist.

Retinal microvascular changes from endothelial dysfunction produce visual disturbances that standard ophthalmic examination does not detect. The retina has one of the highest metabolic demands of any tissue in the body. It depends on dense capillary networks for oxygen delivery. When endothelial dysfunction reduces perfusion through these capillaries, the retinal cells receiving inadequate oxygen generate the symptoms patients describe: intermittent blurring, new floaters, photophobia.

OCT angiography (OCTA) can reveal what the standard exam misses. It maps retinal capillary density and identifies reduced perfusion in the foveal avascular zone. Studies in post-COVID patients show measurable reductions in retinal vessel density correlating with visual complaints.

The eyes are structurally sound. The blood supply feeding the retina is compromised. The testing needs to match the mechanism.

If your vision changed after COVID and your ophthalmologist finds nothing structural, ask about OCT angiography. The technology exists to see what the standard exam cannot.

Volume 6 of The Complete Long COVID Handbook covers endothelial dysfunction, microvascular perfusion, and the specialized testing revealing vascular changes behind "normal" exam results.

03/13/2026

Taking the right supplement at the wrong time can make symptoms worse.

First: magnesium in the morning. Magnesium glycinate has a calming effect on the nervous system and supports sleep architecture. Taking it at 7 AM wastes the sedative benefit. Move it to 60 to 90 minutes before bed. If you need magnesium for daytime muscle cramps, use magnesium malate in the morning and glycinate at night.

Second: B vitamins at night. B-complex vitamins are activating. They support energy metabolism and neurotransmitter production. Taking them after 3 PM can disrupt sleep onset. Move the full complex to morning, ideally with breakfast.

Third: antihistamines only when symptomatic. Patients take H1 and H2 blockers when symptoms flare and skip them when feeling stable. Prophylactic scheduled dosing maintains a lower histamine baseline. Reactive dosing lets the histamine accumulate before attempting to block it. The scheduled approach is more effective for mast cell-driven symptoms.

Fourth: CoQ10 on an empty stomach. CoQ10 is fat-soluble. Absorption drops significantly without dietary fat present. Take it with your largest meal containing healthy fats.

Fifth: probiotics at the same time as antibiotics. The antibiotic eliminates the probiotic organisms before they can colonize. Space them by at least two hours to allow the probiotic to establish before the next antibiotic dose.

Small adjustments in timing can change whether a supplement helps or hinders recovery.

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

03/12/2026

Long COVID patients with testosterone levels looking like they belong to someone 30 years older. Their doctors say the levels are "low normal."

"Low normal" is a range on a lab report.

SARS-CoV-2 can damage testicular tissue through ACE2 receptor expression on Leydig cells. These are the cells responsible for testosterone production. When Leydig cell function is impaired, testosterone output drops. The decline is often gradual enough so standard screening miss the trajectory.

The symptoms overlap with Long COVID: fatigue, brain fog, depression, muscle wasting, reduced exercise tolerance. Unless testosterone is specifically evaluated, the hormonal component is often a second thought.

Total testosterone alone is not enough. Free testosterone reveals how much is biologically active. SHBG (s*x hormone-binding globulin) shows how much is bound and unavailable. LH and FSH distinguish whether the problem originates in the te**es (primary) or the pituitary signaling pathway (secondary). The distinction determines treatment.

Patients dismissed as having "low normal" levels deserve a complete hormonal workup that accounts for age, baseline, and the clinical picture.

Volume 7 of The Complete Long COVID Handbook covers hormonal disruption, ACE2-mediated tissue damage, complete testing protocols, and treatment approaches for testosterone depletion after COVID.

03/12/2026

Long COVID isn't one problem, it's six interconnected mechanisms needing targeted treatment.

At COVID Institute, we use mechanism-based diagnosis to identify what's actually broken: dysautonomia, mitochondrial dysfunction, endothelial damage, gut dysbiosis, mast cell activation, and hormone imbalance. We offer specialized treatments including Stellate Ganglion Block (SGB), Epipharyngeal Abrasive Therapy (EAT), vagus nerve protocols, and comprehensive care for POTS, MCAS, and chronic pain. Virtual consultations available, you don't have to be in Texas to get started.

Schedule your consultation: (214) 390-7557 or visit https://covidinstitute.org

03/12/2026

Endothelial cells regenerate continuously meaning your blood vessels are not permanently damaged. But they can get stuck in a cycle of injury and repair.

This distinction matters. Endothelial dysfunction in Long COVID is not the destruction of blood vessel walls. It is ongoing inflammation exceeding the rate at which the endothelium can regenerate. The lining is being damaged faster than it can rebuild. But the regeneration process never stops.

When the inflammatory drivers are addressed, the balance shifts, reducing the mechanical burden on vessel walls. Immune modulation can lower the inflammatory signaling as endothelial cells regenerate. Nitric oxide support restores the vasodilation capacity the endothelium needs to function.

Flow-mediated dilation testing helps measure this recovery. It measures how blood vessels respond to changes in blood flow. Patients who track this over months can see improvement as the regeneration rate catches up.

This is one of the mechanisms where objective progress is traceable.

The endothelium regenerates. The repair system is intact. The goal is removing the obstacles preventing it from keeping pace with the injury.

Volume 6 of The Complete Long COVID Handbook covers endothelial dysfunction, microclot pathology, nitric oxide support, and the testing that tracks vascular recovery over time.

03/12/2026

You never clenched your jaw before COVID. Now you wake with jaw pain, headaches radiating from your temples, sore teeth from grinding.

Your dentist fits a night guard. It protects the teeth but does not stop the clenching. The muscle tension returns every night. Some days, the jaw aches by mid-afternoon without any nighttime grinding at all.

This is not stress-related bruxism in the traditional sense. The trigeminal nerve, controlling the masseter and temporalis muscles responsible for jaw movement, is modulated by the autonomic nervous system. When the sympathetic branch stays elevated, these muscles remain in a state of low-grade contraction, whether you are conscious of it or not.

The jaw is responding to the nervous system, not to dental alignment or psychological tension. Sympathetic overactivation keeps the muscles engaged the same way it keeps the heart rate elevated, the palms sweating, and the sleep architecture disrupted. The jaw is one more target of a system stuck in overdrive.

Autonomic testing reveals the sympathetic elevation driving the pattern. Treatment addressing the autonomic dysfunction, rather than the jaw alone, resolves the clenching at its source. Patients who have cycled through multiple night guards, Botox injections, and TMJ specialists without relief often find resolution when the autonomic component is identified and treated.

Your jaw is not the problem. Your nervous system is.

Volume 2 of The Complete Long COVID Handbook covers sympathetic overactivation, trigeminal-autonomic connections, and how autonomic dysfunction produces symptoms in unexpected locations.

03/12/2026

A $35 blood test. Your fasting glucose is normal. That does not mean your insulin is.

Standard metabolic panels check fasting glucose and A1C. Both can be completely normal while insulin resistance has been developing for years. The body compensates by producing more and more insulin to keep glucose in range. By the time glucose rises, the dysregulation is advanced.

Fasting insulin is a simple blood draw costing $15 to $35 depending on the lab. It measures the hormone directly rather than relying on the downstream marker glucose.

Here are the steps:

Step one: request fasting insulin along with fasting glucose at your next blood draw. Specify fasting insulin, not just a metabolic panel. Most standard panels do not include it.

Step two: calculate HOMA-IR. The formula is fasting insulin multiplied by fasting glucose, divided by 405. Your doctor can calculate this, or you can do it yourself.

Step three: interpret the result. HOMA-IR below 1.0 is optimal. Between 1.0 and 1.9 suggests early insulin resistance. Above 2.0 indicates significant insulin resistance requiring intervention. Above 2.9 is strongly indicative of metabolic dysfunction.

In Long COVID, insulin resistance drives weight gain resistant to diet changes, fatigue worsening after meals, and brain fog correlating with blood sugar fluctuations. Identifying it early can help change the trajectory.

Volume 7 of The Complete Long COVID Handbook covers insulin resistance, HOMA-IR interpretation, and the metabolic patterns connecting hormonal dysregulation to Long COVID symptoms.