The Vitamin D–Microbiome–Sleep Pathway Remains an Unproven Clinical Hypothesis

Stasha Gominak advances a clinical hypothesis linking vitamin D status, gut-microbiome function, B-vitamin availability, and sleep regulation. In her account, people who cannot sleep restoratively are often dealing with a biochemical deficiency state rather than simply failing at sleep hygiene. She believes the same underlying state can contribute to headaches, pain, mood problems, digestive symptoms, metabolic disease, and neurological illness.

The established evidence is narrower than her full model. Vitamin D deficiency is associated with shorter sleep, poorer sleep quality, awakenings, and some sleep disorders. Animal research suggests vitamin D can affect cholinergic signaling, and some vitamin D trials report improvements in subjective sleep quality. But the claim that low vitamin D makes the brain “forget how to sleep,” or that vitamin D deficiency predictably produces a microbiome-driven B-vitamin deficiency, remains unestablished.

That distinction matters because Gominak’s advice is not simply to take more vitamins. She argues that supplements are biologically active interventions, with effects that can change as a person’s condition changes. In her model, taking vitamin D, B vitamins, or a high-dose multivitamin without a defined reason and without tracking the response can make a person feel worse.

Gominak says she has worked with about 2,000 patients in clinical practice and reached another 5,000 to 6,000 through sleep coaching. The people who came to her, she says, had usually already tried the standard behavioral advice: blackout curtains, a regular bedtime, reduced noise, cooler rooms, and reserving the bedroom for sleep. She does not reject those measures. Her first recommendation is still to use them, and not to add supplements if they solve the problem.

Her attention turned to sleep after a young, thin patient with chronic daily headaches insisted on a sleep study. The patient had sleep apnea and, after beginning CPAP treatment, returned with her headaches resolved. Gominak began ordering more sleep studies in headache patients and neurological patients, looking for an explanation beyond the symptoms that initially brought them to a physician.

Her broader criticism is directed at what she sees as a fragmented medical approach: identifying a condition, assigning it to a specialty, and treating its most immediate symptom. She wants to ask whether poor sleep reflects failure in the body’s overnight repair systems. That is the question from which her vitamin D and microbiome theory follows.

Gominak’s early cases made her doubt that sleep apnea should be understood only as an anatomical airway problem. She had been taught to associate apnea chiefly with older, heavier patients and obvious structural risks. Instead, she saw young women with headaches, fragmented sleep, and abnormal sleep studies. Some described waking around 3 a.m., sleeping lightly through the rest of the night, being unable to return to sleep, or waking with a headache.

Some of those patients did have apnea. Others, Gominak says, had delayed REM sleep, little or no REM sleep, or breathing interruptions that appeared only during REM. The pattern led her away from a purely pulmonary explanation and toward the brain stem, which she describes as the part of the brain regulating autonomic activity during sleep.

A hypnogram shown during the discussion maps repeated cycles across a night: lighter sleep stages, deep or slow-wave sleep, and REM sleep. During REM, the brain remains active while most skeletal muscles are temporarily inhibited. Gominak treats this as a demanding physiological state rather than a passive one. In her account, the sleeping brain stem regulates heart rate, blood pressure, breathing, muscle tone, and transitions among sleep stages.

She describes the sympathetic nervous system as the “fight-flight” system and the parasympathetic system as the “rest and digest” system. In her interpretation, sympathetic activity plays a larger role in the first half of a normal night, while parasympathetic activity becomes more prominent after roughly 3 a.m. Patients with very little late-night REM appeared to her to be missing part of that parasympathetic drive.

REM also became important to her because of what patients reported about mood and memory. People who woke early but could return to sleep often said they felt better the next day. Those who could not might describe irritability, depression, or a sense that they had not recovered overnight. Gominak interprets those experiences as signs of impaired sleep-stage regulation.

The neurotransmitter she identifies is acetylcholine. She says acetylcholine supports parasympathetic signaling, attention during wakefulness, and entry into REM sleep. Her proposed mechanism is that vitamin D activity affects choline acetyltransferase, an enzyme involved in acetylcholine production. If vitamin D is low, she argues, the systems that coordinate REM and autonomic sleep regulation may be compromised.

Gominak began examining vitamin D after testing vitamin D and B12 in roughly 500 patients between September and December 2009. She says vitamin D levels in that group were low. Two patients already using CPAP told her that after starting vitamin D, their sleep improved and their headaches disappeared. Those reports did not establish a causal mechanism, but they led her to investigate whether vitamin D could be relevant to sleep regulation.

She found work by Walter Stumpf describing vitamin D receptors in brain-stem regions involved in REM-related muscle inhibition and in nuclei associated with biological timing. For Gominak, the receptor evidence made vitamin D a plausible candidate for further inquiry: if the relevant brain regions contain vitamin D receptors, she reasoned, then low vitamin D might alter their function.

She considers vitamin D more properly understood as a hormone than as an ordinary dietary vitamin. Her reasoning is that it is made in the skin, acts through cellular receptors and gene expression, and functions within a physiological range in which both too little and too much can matter.

That framing drives her criticism of fixed-dose vitamin D trials. She argues that giving every participant the same dose without accounting for starting levels, season, sun exposure, or achieved blood levels does not test vitamin D as a hormone would normally be managed. In her practice, she says, people required very different doses to reach similar blood levels.

For people with sleep or medical problems, Gominak says she aims to keep vitamin D blood levels above 60. She distinguishes that target from a recommendation for healthy people seeking general optimization, and says her approach requires repeated testing and close attention to symptoms.

The Endocrine Society takes a different position. Its 2024 guidance advises against routine vitamin D testing in otherwise healthy adults without a specific medical need. Gominak reads the lack of definitive dosing evidence as a reason to pursue better individualized studies; the guidance does not endorse her treatment target or her protocol.

Vitamin D did not leave Gominak convinced that she had solved her patients’ problems. Some people initially slept better, she says, but later returned with diffuse joint pain, burning sensations in their hands and feet, agitation, insomnia, or recurring headaches. She began to suspect that correcting one deficiency had increased demand on another system.

Her route to B vitamins began with pantothenic acid, or vitamin B5. A patient brought her a book about B5 while Gominak herself was experiencing buttock pain that made it difficult to sit through the end of a clinical day. She followed the book’s references to older experiments that, as she recounts them, linked pantothenic-acid deprivation to insomnia, gastrointestinal complaints, an abnormal gait, and burning pain in the hands and feet.

B5 is a precursor to coenzyme A, a helper molecule involved in energy metabolism. Gominak links coenzyme A to cortisol production, mitochondrial function, inflammation, and the body’s ability to make energy. She initially recommended high-dose B5 alongside B100, a complex containing all eight B vitamins.

The result reinforced her warning that supplements are not automatically benign. Gominak says 400 milligrams of B5 worsened her own restless legs, while some patients became agitated, sleepless, or achy at that dose. Others did well on lower doses or on a B complex without separate high-dose B5.

In her model, the problem is not that B vitamins are inherently beneficial or harmful. The question is whether a person needs them, at what dose, and for how long. Symptoms that resemble the original complaint—insomnia, pain, restlessness, fatigue—may, she says, arise from too little or too much.

Her explanation centers on the microbiome. Gut microbes can produce, consume, and exchange all eight B vitamins. Gominak describes people and their intestinal microbes as commensal partners: the body provides an environment and growth factors, while microbes provide B vitamins and other compounds in return.

She uses a river analogy. The organisms present in the gut at any moment are constantly reproducing and moving through the digestive tract. Probiotics may add organisms, she says, but may not establish a stable population if the conditions needed for those bacteria to reproduce are absent. She views prebiotics as more conceptually promising because they feed bacteria already present.

The disputed step is her proposed link between vitamin D and microbial B-vitamin production. Gominak’s 2016 hypothesis was that vitamin D deficiency changes the intestinal microbiome, reducing production of B vitamins in the gut. In that model, vitamin D plus all eight B vitamins may restore the microbiome over roughly three months; once microbial production resumes, large B-vitamin doses may become disruptive.

Steven Bartlett raises the central objection. The material he reviewed states that vitamin D supplementation does not cause or drain B vitamins, and that low vitamin D and low B12 often coexist because of shared factors such as restrictive diets, aging, or impaired absorption.

Gominak agrees that her proposed pathway is not represented in conventional literature apart from her own work. She also allows that there may be intermediate mechanisms rather than vitamin D directly “using up” B vitamins. Her claim is ultimately broader: vitamin D may affect the microbiome, the microbiome may affect B-vitamin availability, and B5 availability may influence coenzyme A production.

That model remains a hypothesis. It is the framework through which Gominak interprets the pain, sleep changes, and digestive symptoms she says she observed in patients, but it does not convert those clinical accounts into proof that vitamin D supplementation causes B-vitamin deficiency.

Gominak presents Madeline and Natalie as the clinical accounts that persuaded her to continue pursuing the theory. They are not offered as controlled demonstrations of cause and effect. They are examples of how she says her approach worked in people with very different profiles.

Madeline was 32, a redhead, and about 100 pounds overweight. She had endometriosis, polycystic ovarian syndrome, gestational diabetes, daily headaches, leg pain, burning in her hands and feet, reflux, constipation, frequent nighttime urination, and disrupted sleep. She was taking about nine medications.

Gominak says CPAP improved Madeline’s sleep somewhat but did not resolve the larger symptom cluster. After vitamin D and later B-vitamin interventions, she says Madeline’s leg pain and burning sensations diminished, her sleep improved, her depression resolved, and she stopped three pain medicines. By the third and fourth years of the program, Madeline was preparing to return to work through a Texas-supported program.

Madeline remained substantially overweight. Gominak interprets that as evidence that the body may prioritize repair before weight loss. She says Madeline maintained a vitamin D level in the 60s while taking 30,000 IU daily for four years—an unusually high dose in her practice, which Gominak interprets as evidence that Madeline’s body was using a large amount of vitamin D.

Natalie presented a different picture. She was a tall, athletic triathlete with two children. After her second pregnancy, she developed abnormal sleep, daily headaches, postpartum depression, gestational diabetes, and a high resting heart rate. Gominak emphasizes that Natalie exercised, spent time outdoors, and had tried diets she regarded as health-conscious.

Natalie first slept better after vitamin D, Gominak says, but the improvement stopped after about two years. She then used B50 for three months and later a multivitamin. Gominak says Natalie lost weight, discontinued antidepressants, saw her resting heart rate come down, and returned to triathlon.

The contrast is central to Gominak’s theory. Madeline had a dense cluster of pain, digestive, metabolic, and sleep problems and remained on a high vitamin D dose. Natalie, whom Gominak considered less severely affected, improved with a shorter B-vitamin phase and eventually stopped supplements.

Gominak uses the cases to argue that B50 should be temporary rather than a permanent daily regimen. In her approach, it is a bridge: use it during a period of recovery, move to a lower-dose multivitamin, and eventually stop supplementation if the body appears able to maintain itself.

She also uses the cases to argue for keeping a symptom log. People can forget improvements once symptoms recur, she says, and may miss patterns in headaches, pain, mood, sleep continuity, digestion, or daytime energy. But the log matters equally for adverse changes. Agitation, insomnia, aching, burning sensations, and restlessness are all signals, in her model, that a dose or intervention may be wrong.

Gominak’s RightSleep program translates her model into a staged supplement sequence. The phase chart she presents includes vitamin D throughout, B12 when indicated, B50 for the first three months, a multivitamin later in the program, and additional B5 if needed.

The displayed phases should not be mistaken for a universal supplement schedule. Gominak repeatedly describes the method as variable: B12 is used only when she considers it low, vitamin D doses are adjusted according to blood levels in her system, and B-vitamin dosing is changed according to symptoms.

Her picture of successful sleep is specific: falling asleep around 10 p.m., waking around 6 a.m., returning to sleep after a brief waking, not waking to urinate, waking without pain, and feeling energetic through the day. If sleep improves and later worsens, she says, a participant should not automatically conclude that the approach has failed. In her interpretation, that change may signal a new unmet need.

That is also why she tells people to read supplement labels carefully. Products marketed as multivitamins can contain B-vitamin doses equivalent to B50. In Gominak’s account, the same B vitamins that temporarily help someone can impair sleep or cause agitation once the person no longer needs that dose.

Her first recommendation remains conventional behavioral sleep practice: address darkness, eye coverings or blackout curtains, scheduling, and the rest of standard sleep hygiene before experimenting with supplements.

For diagnosed or severe sleep disorders, she is less optimistic that lifestyle changes alone will be enough. She says people with sleep apnea, narcolepsy, or pronounced sleep disruption may need structured and sometimes professional help. She describes what she considers transition states during recovery: nightmares or awakenings from REM may indicate that someone is entering REM again but has not yet established stable sleep cycling.

Gominak goes further with narcolepsy. She describes a client who stopped smoking, used nicotine patches around the clock, and whom she says “completely cured herself” of narcolepsy. Her rationale is that nicotine can mimic acetylcholine. Evidence for nicotine as a treatment for narcolepsy remains limited and insufficient to support it as an evidence-based clinical treatment.

Steven Bartlett asks why someone should not simply spend more time outside, improve diet, and eat fermented foods rather than begin a supplement protocol. For people without severe problems, Gominak says that is likely the better path.

She does not consider vitamin D supplements equivalent to sunlight. She cites Stephanie Seneff’s hypothesis that vitamin D made in skin may be sulfated and behave differently from supplemental vitamin D. Sulfated vitamin D metabolites are measurable and likely relevant to vitamin D homeostasis, but their direct biological role and Seneff’s broader hypothesis remain unresolved.

Gominak’s larger point is that UVB exposure does more than create vitamin D3 from a cholesterol precursor in the skin. She believes sunlight produces other compounds and provides wavelengths of energy unavailable in a vitamin D pill. She extends that argument to infrared light, which she says penetrates the body and supports mitochondrial energy production. Research on red and near-infrared photobiomodulation often finds increased mitochondrial activity and ATP production, though effects depend heavily on wavelength, dose, duration, and cell context.

Her advice is not to maximize sun exposure. Direct sunlight is required for vitamin D production in skin, she says, but sun exposure should be limited to avoid burning. She says UVA tanning beds may tan skin without producing vitamin D, while window glass prevents vitamin D production. Light cloud cover can still allow some UVB through, although thick cloud can greatly reduce it.

Gominak sees indoor life as the deeper mismatch. She points to air conditioning, computer-based work, sunscreen use, and children spending much of the day indoors. Bartlett cites an estimate that Americans spend about 90% of their time indoors, or roughly 22 hours a day on average. Gominak thinks that pattern has separated people from environmental conditions their biology expects.

Fermented foods are part of her food-first alternative. Kimchi, kombucha, yogurt, sauerkraut, and kefir contain microbial communities and microbial products. She treats them as possible sources of compounds relevant to microbiome function. But she did not make dietary change her main intervention for people with serious sleep problems because she could not predict how quickly or consistently it would work. Her protocol, she says, is faster because it follows patterns she believes she has observed repeatedly.

She does not prescribe one universal diet. Someone whose digestive symptoms improve on a mostly meat-based diet may be supporting one microbial environment, she says, while a predominantly plant-based eater may support another. Her clearest dietary warning is against a prolonged, highly carbohydrate-dependent diet.

She invokes historical cases of beriberi in populations relying heavily on processed rice and pellagra in people fed corn gruel. In her reading, those cases demonstrate that diet can cause nutrient deficiencies and alter the conditions under which gut microbes live. Her practical measure is not adherence to a named diet, probiotic, fermented-food regimen, or supplement stack. It is whether a person sleeps better, digests food more reliably, has less pain, and sustains daytime energy.