Robert Groysman, MD, 6957 W Plano Pkwy, suite 2100, Plano, TX (2026)

04/04/2026

You used to wake up and feel refreshed.

The night had done its job. You got up, moved, started the day.

Now you wake up after eight hours and feel like you never closed your eyes. The sleep tracker says you slept. The symptoms say otherwise. Fatigue before the day begins. Heaviness in the limbs that lifting them does not relieve. Brain that will not engage before noon, and sometimes it stays unengaged.

This is unrestorative sleep, and is a consistent complaint in Long COVID.

The explanation is cellular. When you sleep mitochondria perform maintenance functions that cannot be adequately managed during waking hours. Cellular debris is cleared. Metabolic waste from the previous day's activity is processed. Tissue repair begins. These are energy-dependent processes. If the mitochondria cannot generate sufficient ATP during sleep because mitochondrial function is impaired, the maintenance cycle is incomplete.

You wake up with cell environment that did not finish processing overnight. The fatigue is not from insufficient sleep duration. It is from insufficient cellular restoration during sleep.

This is also why the usual sleep hygiene advice does not change the picture. The problem is not the sleep architecture. It is the cellular work that sleep is supposed to enable.

Volume 3 of The Complete Long COVID Handbook covers mitochondrial dysfunction, unrestorative sleep, and the cellular processes that distinguish sleep duration from sleep quality at the biochemical level.

04/04/2026

Five s*x hormone markers worth understanding in Long COVID evaluation.

Hormone disruption after COVID is common across both s*xes and all ages. These are the markers that provide the most clinical information:

Estradiol (E2)
The primary form of estrogen during reproductive years. In Long COVID, estradiol often drops below what pre-infection levels would have been for that age and cycle phase. Low estradiol correlates with worsening cognitive symptoms, autonomic instability, and sleep disruption. Lab range reference values often accommodate a very wide normal band — a result that reads "normal" may still be significantly below that individual's personal baseline.

Progesterone
Works in balance with estrogen. Low progesterone relative to estrogen creates estrogen dominance, which can worsen MCAS symptoms, mood instability, and sleep problems. Testing should occur in the luteal phase for cycling women to capture the appropriate phase-specific values.

Total and Free Testosterone
Low in both men and women with Long COVID. In men, significant drops correlate with fatigue, cognitive slowing, reduced exercise tolerance, and mood disruption. In women, low testosterone contributes to fatigue, reduced motivation, and pain sensitivity. Free testosterone is the biologically active fraction — total testosterone alone can be misleading.

DHEA-S
An adrenal precursor to s*x hormones. Drops in DHEA-S can signal adrenal dysfunction related to the HPA axis disruption common in Long COVID. Low DHEA-S can impair downstream hormone production even when other levels appear adequate.

S*x Hormone Binding Globulin (SHBG)
Determines how much hormone is actually available to tissues. High SHBG binds hormones and reduces the free fraction available for receptor binding. Testing total hormone levels without SHBG misses the picture of what tissues are actually receiving.

(Consult with your doctor before ordering or interpreting any hormone testing.)

Volume 7 of The Complete Long COVID Handbook covers s*x hormone evaluation in Long COVID, including testing frameworks and what the results mean for treatment direction.

04/04/2026

Estrogen supplementation is not the same as estrogen neuroprotection.

Many Long COVID patients with hormonal disruption are offered standard hormone replacement therapy dosing. The doses are calibrated for managing menopausal symptoms: hot flashes, vaginal atrophy, bone density protection. They are not calibrated for neurological function, cognitive stabilization, or the specific hormonal deficits that accompany post-COVID immune and endocrine disruption.

Estrogen's neuroprotective effects operate through mechanisms that are dose-dependent and receptor-dependent. Estrogen receptors in the hippocampus, prefrontal cortex, and brainstem regulate neurotransmitter synthesis, synaptic plasticity, and neuroinflammatory modulation. These functions require estrogen levels within a range that supports receptor occupancy across these structures.

Standard menopausal HRT dosing may restore peripheral estrogen levels to a range that prevents osteoporosis and manages vasomotor symptoms while leaving neurological receptor sites underoccupied.

This is why Long COVID patients sometimes receive HRT and still experience cognitive fog, mood instability, and worsening neurological symptoms. The hormone has been replaced in name. The neuroprotective coverage may be incomplete.

The evaluation needs to include not just whether hormones are present, but whether they are present at levels that support the neurological functions patients are struggling to recover.

(Consult with your doctor before starting or changing any medication.)

Volume 7 of The Complete Long COVID Handbook covers hormone imbalance, estrogen neuroprotection, and why Long COVID hormonal evaluation requires a different framework than standard menopausal care.

04/03/2026

You are fine in the morning. By 2 PM you cannot hold a thought.

This is not fatigue in the ordinary sense. It is not solved by coffee or a short rest. It is the predictable collapse of a system running on inadequate fuel reserves.

Mitochondrial dysfunction in Long COVID is not uniform across the day. The brain's energy demand is highest during periods of sustained cognitive engagement — processing information, making decisions, tracking conversational threads, reading with comprehension. For patients with mitochondrial dysfunction, ATP production cannot keep pace with this demand indefinitely.

What happens in the afternoon is not random. It is the point at which cognitive energy reserves are depleted. The mitochondria were working at reduced capacity from the start of the day. By afternoon, the debt has accumulated.

The pattern is consistent: morning clarity that degrades predictably, cognitive performance that correlates with physical activity earlier in the day, afternoon fog that is heavier after a demanding morning.

This is not a character trait. It is mitochondrial physiology under load.

The implications are practical. Cognitive tasks requiring quality output need to happen in the first few hours of the day before the reserve is drawn down. Social commitments, medical appointments, complex decisions — placing these in the afternoon predictably produces worse outcomes.

Understanding the mechanism allows you to plan around it rather than be surprised by it.

Volume 3 of The Complete Long COVID Handbook covers mitochondrial dysfunction, cognitive energy demand, and how to structure daily activity around actual energy capacity rather than the schedule you wish you had.

04/03/2026

I get asked every day, is it long COVID?

A simple way to think about timing:
For Long COVID after infection, most major definitions use about 3 months as the key cutoff.

CDC: Long COVID is a chronic condition that occurs after SARS-CoV-2 infection and is present for at least 3 months.

WHO: Symptoms usually start within 3 months of the initial COVID illness and must last at least 2 months.

NICE (UK):
• 4 to 12 weeks = ongoing symptomatic COVID
• Symptoms more than 12 weeks = post-COVID-19 syndrome

So in everyday language, if symptoms are still there around 12 weeks / 3 months after COVID, that fits what most people mean by Long COVID.

What about proving COVID was the cause?

In general, the timing makes the connection stronger when symptoms:
• began during the infection
• or started within days to weeks after it
• or clearly showed up within about 3 months

The farther away symptoms begin from the infection, the harder it becomes to confidently say COVID was the trigger.

What about after the COVID vaccine?

This is different. There is no single official definition for a chronic post-vaccine syndrome that matches the formal Long COVID definitions.

Routine vaccine side effects are usually mild and temporary and generally go away within a few days.

So if someone develops symptoms:
• very soon after vaccination
• and those symptoms continue for weeks to months,
that makes a vaccine-related timing argument stronger.

If symptoms first begin many months later or even a year or more later, it becomes much harder to confidently blame the vaccine based on timing alone.

You can't blame the vaccine if you didn't develop symptoms within the first few weeks post vaccination. Well you can, but I would not.

04/03/2026

Six months ago you could not stand in the shower for more than three minutes without gripping the wall.

Heart rate at 140 just from standing upright. Vision greying at the edges. Sitting down on the shower floor to finish washing your hair.

Today you took a twelve-minute shower. Standing the entire time.

Not because the dysautonomia is gone. Because the autonomic nervous system can be retrained — slowly, carefully, with protocols that respect where it currently is rather than demanding where it used to be.

HRV-guided recovery is one of the more reliable tools we have for tracking autonomic reconditioning. Heart rate variability measures the beat-to-beat variation in cardiac rhythm, and it reflects the balance between sympathetic and parasympathetic nervous system activity. In dysautonomia, HRV is typically suppressed. The sympathetic system is dominant. The parasympathetic cannot adequately modulate it.

As autonomic reconditioning progresses, HRV trends upward. It does not trend linearly. There are setbacks and flares. But the directional movement over weeks and months tells a more accurate story than any single day.

The patient described above is not recovered. She still paces. She still has bad days. But the shower is no longer the hardest part of her morning.

That is what progress looks like in dysautonomia. Not a dramatic reversal. A slow, measurable reclaiming of ordinary things.

Volume 2 of The Complete Long COVID Handbook covers dysautonomia, autonomic reconditioning, HRV-guided recovery, and pacing protocols designed for where patients actually are.

04/03/2026

SIBO, MCAS, and dysbiosis can produce nearly identical gut symptoms. How do you tell them apart?

All three can cause bloating, abdominal pain, food intolerance, nausea, and irregular bowel patterns. The distinguishing features are in the triggers, timing, and associated symptoms.

SIBO (Small Intestinal Bacterial Overgrowth) - Strongly food-dependent. Bloating begins thirty to ninety minutes after eating and peaks one to two hours in. Carbohydrates and fermentable foods are the primary triggers. Breath testing after lactulose or glucose challenge will often be abnormal. Symptoms are mostly digestive and do not involve skin, heart rate, or neurological changes.

MCAS (Mast Cell Activation Syndrome) - Can extend beyond the gut. Food triggers gut symptoms AND non-gut symptoms including flushing, heart rate surges, brain fog, itching, or hives. The reaction can begin within minutes of exposure. High-histamine foods are common triggers (aged cheeses, fermented foods, wine, tomatoes, spinach). Tryptase, histamine, and prostaglandin D2 testing can support the diagnosis.

Gut Dysbiosis (Microbiome Imbalance) - Slower and more diffuse than SIBO or MCAS. Symptoms are less acute and more persistent: low-grade bloating throughout the day, irregular bowel habits, increased sensitivity to previously tolerated foods. Stool microbiome testing and intestinal permeability markers are the primary investigative tools.

The overlap is real. Many Long COVID patients have more than one of these simultaneously. Testing across all three pathways produces a more complete picture than treating the most obvious presentation alone.

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

Volume 4 of The Complete Long COVID Handbook covers gut dysbiosis, and Volume 5 covers MCAS and histamine intolerance.

04/03/2026

NSAIDs target inflammation. Long COVID neuropathic and fatigue-related pain isn't always an inflammation problem. It can be an energy production problem.

Ibuprofen, naproxen, aspirin. Non-steroidal anti-inflammatory drugs work by inhibiting COX enzymes, reducing the production of prostaglandins and other inflammatory mediators. For acute injury, post-surgical inflammation, or musculoskeletal conditions where prostaglandin-driven inflammation is the primary mechanism, NSAIDs are effective.

In Long COVID, the pain link is different. Widespread muscle aching does not respond to normal anti-inflammatory dosing. Burning sensations in the extremities. Sensitivity to touch and pressure that fluctuates with activity level. Fatigue and pain worsening, then peaking twelve to forty-eight hours after exertion.

This pattern of pain does not reflect localized inflammatory damage. It reflects peripheral nerve dysfunction in the context of cellular energy failure. Mitochondria in peripheral nerve cells cannot maintain the energy needed to sustain normal nerve function. The nerves report the deficit as pain.

NSAIDs do not address ATP production. They do not support mitochondrial function. They do not restore the energy supply to peripheral nerves.

Patients who take anti-inflammatories regularly and still hurt are not being stubborn. They are using the right tool for the wrong mechanism. The pain is real. The biological driver is probably not inflammatory in the way NSAIDs are designed to address.

(Consult with your doctor before starting or changing any medication.)

Volume 3 of The Complete Long COVID Handbook covers mitochondrial dysfunction, neuropathic pain in the context of energy failure, and targeted approaches that address the underlying mechanism.

04/02/2026

Your vision changed after COVID and your eye exam came back normal.

Ophthalmology checked refraction, intraocular pressure, retinal health. Everything measured correctly. You were told your eyes are fine.

Your eyes may be fine. The vascular supply to your visual processing system may not be.

Visual symptoms in Long COVID follow a distinct pattern that standard eye exams are not designed to detect. Blurring that comes and goes throughout the day. Difficulty focusing on text after sustained reading. Light sensitivity that was not present before infection. Visual field disturbances, floaters, and the sense that your vision has shifted even when the eye itself has not changed.

These symptoms are consistent with endothelial dysfunction affecting the microvasculature of the optic nerve, retinal capillaries, and the posterior cerebral circulation supplying visual cortex.

The endothelium lining those capillaries produces nitric oxide to regulate blood flow. When COVID damages the endothelium, perfusion to small vessels becomes unreliable. Optic nerve function, like vestibular function, degrades when its vascular supply becomes inconsistent.

The distinction matters because the treatment approach is entirely different. Updating your glasses prescription addresses a refraction problem. Addressing microvascular dysfunction addresses the underlying mechanism. If the eye exam is normal and the symptoms persist, the investigation has not reached the right layer.

Volume 6 of The Complete Long COVID Handbook covers endothelial dysfunction, the microvasculature of the nervous system, and why normal ophthalmological exams do not rule out visual involvement in Long COVID.

04/02/2026

You filed for disability. Your IME was twelve minutes long.

The insurance-appointed physician spent less time with you than it takes to watch a sitcom cold open. Your chart was reviewed, questions were asked, and a determination was made that you were capable of returning to work.

Independent medical examinations in disability cases are often structured to produce a predetermined outcome. The physician is not your doctor. They have no treatment relationship with you, no longitudinal knowledge of your history, and no stake in your recovery. They are paid to assess you in a fixed window of time.

Twelve minutes cannot capture dysautonomia that worsens after standing for twenty minutes. It cannot document the cognitive deterioration that begins two hours into sustained mental effort. It cannot assess post-exertional malaise that arrives twenty-four to forty-eight hours after exertion, well after the examination ends.

The IME captures a snapshot. Long COVID is a fluctuating, time-dependent, effort-dependent condition. The examination methodology is designed for acute or stable conditions. It is not designed for what you have.

This is not a failure of medicine. It is a failure of the system in which medicine is being applied. Your test results, your treatment records, and your clinician's documentation contain more information than twelve minutes allows any examiner to process.

The IME denial is not evidence that your condition is not real. It is evidence that the evaluation format is insufficient for the condition being evaluated.

Volume 1 of The Complete Long COVID Handbook covers the multi-system nature of Long COVID and why comprehensive evaluation requires longitudinal clinical assessment rather than single-session examination.

04/01/2026

You used to sleep through the night without thinking about it. Lights out at 11, alarm at 7.

Now you are wide awake at 2 AM. Not anxious. Not worried about anything. Just awake, heart beating slightly too fast, mind not racing but not quiet either. You lie there for an hour. Sometimes two. You finally fall back asleep at 4. The alarm goes off at 7 and you feel like you never slept at all.

This has been happening for months.

Your doctor orders a sleep study. Results are normal. You are told to improve your sleep hygiene.

What the sleep study does not capture is what is happening hormonally at 2 AM. Cortisol and estrogen have a reciprocal relationship in sleep regulation. Estrogen supports the production of serotonin, which converts to melatonin. It also modulates cortisol sensitivity at the cellular level.

When estrogen drops — through menopause, post-COVID hormonal disruption, or stress-induced suppression — cortisol no longer has the same buffering. The cortisol surge that naturally occurs in the early morning hours, designed to prepare the body for waking, arrives too early and too strongly. It tips you out of sleep at 2 or 3 AM when the estrogen buffer is no longer there to modulate it.

This is not insomnia in the conventional sense. Sedating the brain does not fix a hormone regulation problem. The 2 AM waking is a symptom of an underlying endocrine disruption that standard sleep studies are not designed to find.

Volume 7 of The Complete Long COVID Handbook covers hormone imbalance after COVID, including the cortisol-estrogen relationship, 2 AM waking patterns, and how targeted hormone evaluation changes the approach to post-COVID sleep disruption.

04/01/2026

Your hands turn white in a cold grocery store. Purple when you stand in line too long. Red and burning when you get home and warm up.

Before COVID, this never happened.

Now your extremities cycle through colors like a mood ring. Your doctor checks circulation. Pulses are fine. ABI is normal. You are told there is nothing wrong with your vascular system.

The vascular system has two layers of function. Large-vessel flow, which those tests measure, and microvascular regulation, which they do not.

Endothelial dysfunction operates at the capillary level. The endothelium, the single-cell lining of every blood vessel, produces nitric oxide to regulate dilation and constriction in the smallest vessels. When COVID damages the endothelium, nitric oxide production drops. The microvascular system loses its ability to regulate blood flow in response to temperature, gravity, and positional changes.

Cold triggers vasospasm in damaged vessels. Standing triggers pooling. Warming triggers reactive hyperemia that overshoots because the regulatory system cannot modulate it.

The colors are not cosmetic. They are a visible map of microvascular dysfunction.

Volume 6 of The Complete Long COVID Handbook covers endothelial dysfunction, Raynaud-like phenomena after COVID, and the specialized vascular testing that captures what standard circulation tests miss.

Robert Groysman, MD

04/04/2026

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