HoldsUp

The Diary Of A CEO · 2026-07-27 · Steven Bartlett (host), Stasha Gominak

Vitamin D Expert: The Supplement World Is Giving The WRONG Advice! | Dr Stasha Gominak

57 research-tied claims examined: 12 contradicted 1 overstated 5 context 35 supported 4 unverified

12 Contradicted by research
0:10:45Stasha Gominakcontradictedhigh

All animals, including fruit flies, experience paralysis during sleep.

"And it turns out every animal, including fruit flies, who we're doing sleep studies on, get paralyzed in sleep." (said at 0:10:45)

The claim that 'every animal, including fruit flies... get paralyzed in sleep' is contradicted by comparative sleep biology. Muscle atonia (motor paralysis) is a specific physiological feature of rapid eye movement (REM) sleep found primarily in terrestrial mammals, birds, and certain reptiles. In invertebrates like Drosophila (fruit flies), sleep is characterized by behavioral quiescence, increased arousal thresholds, and posture regulation, not active neuromuscular paralysis/atonia. Furthermore, several vertebrate species—most notably cetaceans (such as dolphins and whales) and certain birds—exhibit unihemispheric slow-wave sleep, during which they continuously maintain motor activity, posture, swimming, or flight, demonstrating that sleep across the animal kingdom does not universally involve paralysis.

0:13:20Stasha Gominakcontradictedhigh

The first half of the night until about 3:00 a.m. is predominantly governed by the sympathetic nervous system.

"The first half of the night till about 3:00 a.m. is mostly run by the sympathetic side." (said at 0:13:20)

The speaker gets the autonomic nervous system physiology backwards. Normal nocturnal sleep, particularly the first half of the night, is dominated by non-rapid eye movement (NREM) and slow-wave sleep (SWS), which is characterized by maximal parasympathetic (vagal) dominance and a significant suppression of sympathetic nervous activity. Sympathetic activity is lowest during deep slow-wave sleep (typically peaking in occurrence in the early part of the night) and shifts toward higher sympathetic modulation during REM sleep and the early morning hours.

0:14:05Stasha Gominakcontradictedmoderate

The second half of the night, from 3:00 a.m. to 7:00 a.m., is governed by the parasympathetic nervous system.

"The second half of the night, from 3:00 a.m. to 7:00 a.m., is run by the parasympathetic side." (said at 0:14:05)

The speaker gets the autonomic architecture of sleep backwards. In healthy sleep, the first half of the night is dominated by non-rapid eye movement (NREM) slow-wave sleep, which exhibits maximum parasympathetic (vagal) tone and reduced sympathetic activity. In contrast, the second half of the night (roughly 3:00 a.m. to 7:00 a.m.) is characterized by longer rapid eye movement (REM) sleep periods and a circadian transition toward awakening, during which parasympathetic dominance decreases and sympathetic tone and heart rate increase, reaching maximal sympathetic modulation in the early morning.

  • contradicts: Autonomic activity during human sleep as a function of time and sleep stage. (Journal of sleep research 2001) · cited 21x in the literature
    "During non-rapid eye movement (NREM) sleep autonomic balance shifted from sympathetic to parasympathetic dominance, although this appeared to be more because of a shift in parasympathetic nervous system (PNS) activity. Autonomic balance during REM was in general similar to wakefulness." (abstract, results, passage verified)
    pubmedfull study (doi)
  • contradicts: Circadian variation of heart rate variability across sleep stages. (Sleep 2013) · cited 236x in the literature
    "The current study revealed that sleep onset and progression to deeper sleep stages was associated with a shift toward greater parasympathetic modulation, whereas rapid eye movement (REM) sleep was associated with a shift toward greater sympathetic modulation. We found a circadian rhythm of heart rate (HR) and high-frequency power during wakefulness and all non-REM sleep stages. A significant circadian rhythm of HR and sympathovagal balance of the heart was also observed during REM sleep. During slow wave sleep, maximal parasympathetic modulation was observed at ~02:00, whereas during REM sleep, maximal sympathetic modulation occurred in the early morning." (abstract, results, passage verified)
    pubmedfull study (doi)
0:16:20Stasha Gominakcontradictedhigh

There are no pharmacological drugs that duplicate the neurotransmitter acetylcholine.

"And the reason why they don't know it is because there are no drugs that duplicate acetylcholine. There are no drugs." (said at 0:16:20)

The claim that there are no pharmacological drugs that duplicate (mimic) the neurotransmitter acetylcholine is contradicted by established pharmacology. An entire class of medications, known as direct-acting cholinergic agonists or cholinomimetics (e.g., bethanechol, pilocarpine, cevimeline, carbachol, and xanomeline), directly bind to and activate acetylcholine receptors (both muscarinic and nicotinic), thereby replicating the physiological effects of acetylcholine.

0:24:10Stasha Gominakcontradictedhigh

Attention deficit hyperactivity disorder (ADHD) was first described in the 1980s.

"non-alcoholic fatty liver was first described in the '80s, ADHD similar." (said at 0:24:10)

Attention deficit hyperactivity disorder (ADHD) was not first described in the 1980s. Historical and medical records document clear clinical descriptions of the syndrome centuries earlier. The earliest known medical descriptions of attention disorders were published by Melchior Adam Weikard in 1775 and Sir Alexander Crichton in 1798, followed by Sir George Frederic Still's foundational clinical lectures in 1902. While the American Psychiatric Association introduced the specific diagnostic terms 'Attention Deficit Disorder' (ADD) in the DSM-III (1980) and 'ADHD' in the DSM-III-R (1987), the clinical syndrome itself was recognized and described long before the 1980s.

0:41:21Stasha Gominakcontradictedmoderate

Furred animals obtain vitamin D by licking their fur where it is synthesized, whereas humans and domesticated pigs synthesize and absorb it directly through skin.

"It is made on our skin. Now, it turns out animals frequently lick their fur, and they get their vitamin D that's made in their fur from licking their fur. Some of it's absorbed, but the thing that's unique about us and pigs, domesticated pigs, is we're bald. That means most of the time we're making it on our skin. It's never supposed to be from the food. It was not ever about the food for us. We don't lick our skin. Therefore, we absorb it through our skin." (said at 0:41:21)

The speaker repeats an old hypothesis that furred animals produce vitamin D in sebum on their fur and ingest it via grooming, while humans and pigs are unique in synthesizing and absorbing it directly through the skin. However, experimental research in hair-covered mammals (such as dairy cows) demonstrates that vitamin D3 is synthesized directly in the skin across the entire body surface despite hair coverage and enters circulation directly, refuting the grooming/licking model. Additionally, obligate carnivores like dogs and cats have negligible cutaneous synthesis due to low 7-dehydrocholesterol and rely strictly on dietary intake.

1:01:50Stasha Gominakcontradictedhigh

The B vitamins were originally identified and described scientifically as bacterial growth factors.

"It turns out that the eight B vitamins were first described as bacterial growth factors." (said at 1:01:50)

The claim that all eight B vitamins were first described as bacterial growth factors is historically inaccurate. The earliest B vitamins (such as thiamine/vitamin B1, niacin/vitamin B3, and riboflavin/vitamin B2) were discovered through animal feeding studies and human nutritional deficiency diseases (such as beriberi and pellagra), notably beginning with Christiaan Eijkman's work in chickens and Casimir Funk's isolation of the antiberiberi factor ('vitamine'). While microbiological nutrition studies (such as those by Esmond E. Snell and Roger J. Williams) were instrumental in discovering or isolating certain B vitamins and cofactors (such as folic acid, pantothenic acid, and biotin) using bacteria and yeast, the group of eight B vitamins as a whole was not first identified as bacterial growth factors.

1:10:10Stasha Gominakcontradictedhigh

Human breast milk contains vitamin D and all eight B vitamins derived from the mother's microbiome.

"mom was giving you D in her breast milk, and it also had eight Bs. Those eight Bs came from her normal microbiome in the breast milk." (said at 1:10:10)

While human breast milk does contain vitamin D (typically at low concentrations) and all eight B vitamins (thiamine, riboflavin, niacin, pantothenic acid, B6, biotin, folate, and B12), the assertion that these B vitamins originate from the mother's milk microbiome is biologically incorrect. Systematic reviews and lactation physiology demonstrate that B vitamins in human milk are derived from maternal circulation, strongly reflecting maternal dietary intake, nutritional status, and supplementation, which are actively transported into milk by mammary epithelial cells rather than synthesized by bacteria inhabiting breast milk.

1:42:18Stasha Gominakcontradictedhigh

LED light bulbs do not emit infrared light energy.

"Now, you'll get halogen or LEDs and they do not give off infrared light energy." (said at 1:42:18)

The speaker bundles two lighting technologies together, claiming that 'halogen or LEDs... do not give off infrared light energy'. This statement is contradicted regarding halogen bulbs, although partially accurate for standard household LEDs: 1. Halogen bulbs: Halogen lamps are incandescent thermal radiators that emit light by heating a tungsten filament. The majority of their optical radiation is emitted in the infrared spectrum (near-infrared and thermal IR), directly contradicting the claim. 2. LED bulbs: Standard white domestic LEDs generate light via electroluminescence (typically a blue LED chip coated with a phosphor) and emit almost entirely within the visible spectrum (approx. 400–700 nm), giving off virtually no infrared optical radiation. Because the statement bundles halogen lamps and LEDs into a single assertion that neither emits infrared energy, the overall claim is judged contradicted by its inaccurate component.

1:52:14Stasha Gominakcontradictedhigh

Nicotine mimics the action of acetylcholine at receptors, which regulates focus and attention during the day and REM sleep at night.

"Because there is only one drug that duplicates acetylcholine completely and it's nicotine. So she stopped smoking and she uses nicotine patches. Nicotine is the duplicate of acetylcholine. Acetylcholine allows us to focus, pay attention, be distracted and come right back during the day. It is in control of our ability to concentrate. At night, it allows us to get into REM sleep." (said at 1:52:14)

The speaker's statement bundles two assertions. The claim regarding acetylcholine's physiological roles is supported: acetylcholine is well established in regulating attention, arousal, and cognitive focus during wakefulness via basal forebrain and brainstem projections, as well as promoting REM sleep via the mesopontine cholinergic system (pedunculopontine and laterodorsal tegmental nuclei). However, the claim that nicotine 'duplicates acetylcholine completely' and is 'the only drug that duplicates acetylcholine completely' is pharmacologically incorrect. Acetylcholine acts on two distinct receptor families: ionotropic nicotinic acetylcholine receptors (nAChRs) and metabotropic muscarinic acetylcholine receptors (mAChRs). Nicotine selectively activates nicotinic receptors and does not activate muscarinic receptors, meaning it does not completely mimic endogenous acetylcholine.

1:52:50Stasha Gominakcontradictedmoderate

Parkinson's disease patients who smoked tobacco have demonstrated better outcomes because Parkinson's disease is primarily an acetylcholine deficiency state.

"It turns out, oddly enough, the guys with Parkinson's disease who smoked throughout the last 30 years have been shown to do better because Parkinson's disease is an acetylcholine deficiency state first." (said at 1:52:50)

The speaker conflates epidemiological observations about Parkinson's disease (PD) incidence with disease progression and misstates the underlying neurotransmitter pathology. While historical epidemiological studies have consistently shown an inverse association between tobacco smoking and the risk/incidence of developing Parkinson's disease, published research on PD patients shows that smoking does not improve clinical outcomes and is instead associated with increased mortality and accelerated cognitive decline. Furthermore, PD is fundamentally defined by the degeneration of dopaminergic neurons in the substantia nigra pars compacta leading to dopamine depletion (whereas primary acetylcholine deficiency is central to Alzheimer's disease pathology, and loss of striatal dopamine actually leads to relative cholinergic hyperactivity, which is why anticholinergics were historically used to treat PD symptoms).

1:35:31Stasha Gominakcontradictedhigh

The first descriptions of vitamin deficiency states occurred in the 1940s in populations consuming pure carbohydrate diets, including Japanese prisoner-of-war camps and the Bataan Death March during World War II.

"There are two incidences from the 1940s where the first vitamin deficiency states were described and both of them turn out to be purely carbohydrate diets. One of them was in the Japanese prisoner of war camps and the Bataan Death March in World War II where they had rice, rice, rice." (said at 1:35:31)

The claim that the first descriptions of vitamin deficiency states occurred in the 1940s (in WWII Japanese POW camps / the Bataan Death March) is contradicted by the history of medicine. Vitamin deficiency diseases and their dietary causes were described and studied decades to centuries earlier. Scurvy (vitamin C deficiency) was experimentally investigated by James Lind in 1747. Beriberi (thiamine/vitamin B1 deficiency) was famously linked to white rice diets and prevented in the Japanese Navy by Kanehiro Takaki in the 1880s, experimentally elucidated by Christiaan Eijkman in the 1890s (work that received a Nobel Prize in 1929), and the term 'vitamine' was coined by Casimir Funk in 1912. By the 1930s, most major vitamins had already been isolated and chemically synthesized.

1 Overstated
1:01:00Stasha Gominakoverstatedmoderate

All eight B vitamins are synthesized by human intestinal bacteria and can be absorbed by the host.

"These eight chemicals called B, all of them are made by bacteria and we absorb them." (said at 1:01:00)

While human intestinal bacteria possess biosynthetic pathways capable of producing all eight B vitamins (B1, B2, B3, B5, B6, B7, B9, and B12), they cannot all be meaningfully absorbed by the human host. Most bacterial synthesis occurs in the colon. Although the colon possesses transporters capable of absorbing several B vitamins (such as biotin, thiamin, folate, and riboflavin), it cannot absorb bacteria-synthesized vitamin B12. Physiological absorption of vitamin B12 requires gastric intrinsic factor and takes place exclusively in the terminal ileum, upstream of where most colonic bacterial B12 synthesis occurs; hence, colonic B12 is excreted in feces and unavailable to humans without coprophagy, requiring dietary intake.

5 Needs context
0:14:35Stasha Gominakneeds contextmoderate

Permanent memory formation occurs during REM sleep.

"Isn't there a body of literature about memory being made permanent during REM? Yes, memory is linked and mood is linked." (said at 0:14:35)

The speaker claims there is a body of literature showing memory is made permanent during REM sleep, and that memory and mood are linked. In sleep neurobiology, long-term memory formation (systems consolidation) is heavily established as occurring during sleep, but the primary transfer of declarative memories to permanent neocortical storage is predominantly driven by slow-wave / non-REM (NREM) sleep via hippocampal-neocortical replay (sharp-wave ripples, slow oscillations, and spindles). REM sleep contributes distinctly to emotional memory processing, mood regulation, schema integration, and procedural memory consolidation rather than being the sole or primary phase where memories are made permanent.

0:43:31Stasha Gominakneeds contextmoderate

Sunscreen use blocks the skin's ability to synthesize vitamin D.

"If you tell them that they can use sunscreen wisely, and it blocks the ability to make vitamin D" (said at 0:43:31)

Sunscreen filters UVB radiation, which is required for cutaneous vitamin D3 synthesis. In controlled experimental and in vitro conditions, proper sunscreen application substantially abrogates vitamin D3 production. However, in real-world practice and field trials, regular sunscreen use has a modest or negligible impact on circulating 25(OH)D levels (or causes only small reductions, around 2 ng/mL), largely because people typically apply less than the recommended thickness, do not reapply frequently, or experience incidental sun exposure.

0:46:19Stasha Gominakneeds contextmoderate

Coenzyme A is required for the biosynthesis of cortisol in the human body.

"Coenzyme A is responsible for making cortisol." (said at 0:46:19)

Coenzyme A (CoA, derived from pantothenic acid/vitamin B5) is fundamentally required for cellular metabolism and de novo cholesterol synthesis via acetyl-CoA and 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA), as well as fatty acyl-CoA utilization and cholesterol ester storage in adrenal tissue. Because cholesterol is the obligatory precursor for steroidogenesis, CoA is necessary upstream for substrate provision. However, the enzymatic cascade directly converting cholesterol into cortisol within the adrenal cortex is mediated by steroidogenic cytochrome P450 enzymes (e.g., CYP11A1, CYP17A1, CYP21A2, CYP11B1) and hydroxysteroid dehydrogenases using NADPH and oxygen, rather than CoA acting as the primary steroid-synthesizing agent.

1:32:26Stasha Gominakneeds contextmoderate

When UVB light strikes cholesterol in the skin, 15 to 20 other photoproduct chemicals are synthesized alongside vitamin D3.

"Number two, it turns out there's a lot of literature that shows that vitamin D is not the only thing made by UVB hitting your skin. And what it's hitting is cholesterol. And that cholesterol is changed as a chemical called D3. But there are probably 15, 20 other chemicals that are being made at the same time." (said at 1:32:26)

The speaker's statement is broadly accurate regarding photochemistry, but simplifies key biochemical details. UVB radiation in the skin primarily strikes 7-dehydrocholesterol (7-DHC, an immediate precursor in cholesterol biosynthesis located in epidermal cell membranes), rather than mature cholesterol itself. Upon UVB exposure, 7-DHC photolyzes into previtamin D3, which thermally isomerizes into vitamin D3. Previtamin D3 and vitamin D3 undergo further photochemical and enzymatic reactions forming numerous photoisomers and metabolites (such as lumisterol, tachysterol, suprasterols, toxisterols, and CYP11A1-derived hydroxyderivatives), amounting to over a dozen distinct photoproducts.

1:47:04Stasha Gominakneeds contexthigh

Pellagra is a niacin deficiency caused by pure corn gruel diets in institutionalized populations in the southern United States in the 1930s and 1940s.

"The same thing about pellagra, which is actually a niacin deficiency in adults and children that were institutionalized in the South of the United States in the '30s and '40s and fed corn gruel as their only food." (said at 1:47:04)

Pellagra is established to be caused by a dietary deficiency of niacin (vitamin B3, or its precursor tryptophan), famously linked to maize/corn-dominated diets lacking bioavailable niacin. In the American South, major epidemiological investigations in institutionalized populations (such as orphanages, mental hospitals, and prison farms) were conducted primarily by Joseph Goldberger between 1914 and the late 1920s, demonstrating that the corn-heavy, monotonous diets caused the disease and dietary diversification cured it. Niacin was identified as the curative factor in 1937, leading to mandatory flour and cornmeal enrichment programs in the 1940s. The claim correctly identifies the biochemical cause (niacin deficiency), dietary cause (corn-based diet), and setting (institutionalized and impoverished populations in the Southern United States), though the primary epidemic and institutional experiments peaked in the 1910s–1920s rather than originating solely in the 1930s–1940s.

35 Supported by research
0:01:32Stasha Gominaksupportedhigh

Vitamin D functions biologically as a hormone rather than a true vitamin.

"one of the interesting things I learned was vitamin D is a hormone. There was a mistake made in calling it a vitamin." (said at 0:01:32)

The speaker's statement is biologically and historically supported. Vitamin D was historically misclassified as a dietary vitamin when it was discovered as an antirachitic nutritional factor in the early 20th century. However, established endocrinological and biochemical consensus recognizes that vitamin D is synthesized endogenously in the skin via photochemical conversion of 7-dehydrocholesterol upon UV exposure and functions biologically as a secosteroid prohormone. It is sequentially converted to 25-hydroxyvitamin D and its active hormonal form, 1,25-dihydroxyvitamin D (calcitriol), which acts via nuclear vitamin D receptors (VDR) to regulate transcription and endocrine/paracrine signaling across multiple organ systems.

0:16:35Stasha Gominaksupportedvery low

Vitamin D produces or upregulates the enzyme that synthesizes acetylcholine.

"what we found out together was that vitamin D makes the enzyme or the protein that makes a certain reaction happen that makes acetylcholine." (said at 0:16:35)

Preclinical animal research demonstrates that active vitamin D (1,25-dihydroxyvitamin D3 / calcitriol) upregulates the activity and expression of choline acetyltransferase (CAT/ChAT), the enzyme responsible for acetylcholine biosynthesis in discrete brain regions. Because the evidence supporting this mechanism is based on animal and laboratory models, certainty is graded as very low.

0:16:52Stasha Gominaksupportedhigh

Heart rate variability increases as the parasympathetic nervous system becomes dominant.

"If you're wearing a sleep tracker, you'll see that there's a measure of what's called heart rate variability that goes up as the parasympathetic becomes dominant." (said at 0:16:52)

The claim accurately reflects established autonomic physiology. Short-term heart rate variability (HRV) metrics, particularly time-domain measures like RMSSD and frequency-domain measures like high-frequency HRV (HF-HRV), predominantly reflect cardiovagal (parasympathetic) outflow. As parasympathetic activity increases or becomes dominant (e.g., during restful sleep, relaxation, or recovery), HRV increases.

0:24:35Stasha Gominaksupportedhigh

Non-alcoholic fatty liver disease was first described in the 1980s.

"non-alcoholic fatty liver was first described in the '80s, ADHD similar." (said at 0:24:35)

Non-alcoholic fatty liver disease (specifically nonalcoholic steatohepatitis, NASH) was first formally described and named as a distinct clinical and pathological entity in 1980 by Dr. Jürgen Ludwig and colleagues at the Mayo Clinic in their landmark paper 'Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease'.

0:09:00Stasha Gominaksupportedhigh

Muscle paralysis (atonia) is most pronounced during rapid eye movement (REM) sleep.

"We get the most paralyzed of all in REM sleep." (said at 0:09:00)

The claim is supported. Muscle atonia (paralysis of postural skeletal muscles mediated by glycinergic and GABAergic postsynaptic inhibition of somatic motoneurons) is a defining neurophysiological characteristic of rapid eye movement (REM) sleep. While non-REM sleep exhibits decreased muscle tone (hypotonia), motor output is most strongly suppressed during REM sleep.

0:11:00Stasha Gominaksupportedhigh

EEG brain wave patterns recorded during REM sleep closely resemble those recorded during wakefulness.

"the waveforms that they record from up here look the same in rapid eye movement sleep as they do in wake" (said at 0:11:00)

The claim is supported. In clinical neurophysiology and sleep medicine (such as AASM standard scoring criteria), electroencephalography (EEG) during rapid eye movement (REM) sleep is defined by low-voltage/low-amplitude, high-frequency, desynchronized 'mixed frequency' activity that closely resembles the EEG patterns of active, alert wakefulness. This hallmark similarity is the primary reason REM sleep was historically designated 'paradoxical sleep'—the brain's electrical activity appears awake despite the individual being in deep sleep with muscle atonia.

0:16:20Stasha Gominaksupportedhigh

Acetylcholine is the primary neurotransmitter used by the parasympathetic branch of the autonomic nervous system.

"Acetylcholine is the neurotransmitter, the chemical that the autonomic parasympathetic side uses." (said at 0:16:20)

Acetylcholine is established in basic neuroscience and physiology as the primary neurotransmitter utilized by the parasympathetic division of the autonomic nervous system, released by both preganglionic and postganglionic parasympathetic neurons.

0:32:37Steven Bartlett (host)supportedmoderate

During sleep at night, the brain undergoes a glymphatic cleaning process that washes away waste products to restore normal function and prevent disease.

"When you go to sleep at night, these cleaners—again, I'm animating this in a way that's not scientifically accurate, but these cleaners come out and clean up your brain. They wash it all and they clean it and they scrub it and they make it all back to normal again. So, if you're not sleeping, then you're going to get some kind of buildup of crap. And that could lead to disease or, you know, other worse things down the line." (said at 0:32:37)

The host's colloquial description accurately summarizes the scientific consensus regarding the glymphatic system. Research demonstrates that glymphatic clearance—a brain-wide perivascular pathway that facilitates the exchange of cerebrospinal fluid and interstitial fluid to clear metabolic waste products (such as amyloid-beta)—is markedly enhanced during sleep and suppressed during wakefulness. Disruption of sleep impairs this clearance pathway, promoting the accumulation of neurotoxic metabolites associated with neurodegenerative diseases.

0:35:54Stasha Gominaksupportedvery low

Walter Stumpf published scientific articles demonstrating that vitamin D receptors are present in the brainstem nucleus responsible for sleep motor paralysis and in circadian clock nuclei.

"Walter Stumpf, S-T-U-M-P-F, who's been writing about vitamin D for 30 years, who has actually published that there are vitamin D receptors in this little stripe along the back of the brainstem that paralyzes us. Like, he knows the name of this nucleus. He has shown articles where the vitamin D receptors are in this nucleus that paralyzes us and in the nuclei that are the clock nuclei that determine what time it is, what time we go to sleep, when we make these transitions." (said at 0:35:54)

The speaker accurately describes the published anatomical autoradiography studies of Walter E. Stumpf and colleagues. Using radiolabeled 1,25(OH)2 vitamin D3 in rodents, Stumpf published multiple landmark papers demonstrating specific nuclear vitamin D receptor binding in brainstem nuclei (including cranial motor nuclei, reticular formation, raphe nuclei, parabrachial nuclei, and pontine nuclei) as well as hypothalamic and forebrain nuclei involved in central regulatory pathways. Because these findings come from preclinical animal autoradiography mapping studies, the body of evidence certainty is rated very low.

  • supports: Nuclear receptor sites for vitamin D-soltriol in midbrain and hindbrain of Siberian hamste… (Histochemistry 1992) · cited 48x in the literature
    "Labeled neurons of varying intensity were found throughout the brainstem in distinct populations at characteristic topographical sites, which include cranial nerve motor nuclei, the nucleus (n.) reticularis tegmenti pontis, the caudoventral region of the n. raphe dorsalis, the n. trapezoides, the n. vestibularis lateralis and n. vestibularis superior, neurons in the various nuclei of the sensory trigeminus, accessory optic nuclei, scattered neurons in nuclei of the reticular formation, the n. ambiguus, certain cells in the area postrema, and many others." (abstract, results, passage verified)
    pubmedfull study (doi)
  • supports: 1,25 (OH)2 vitamin D3 sites of action in the brain. An autoradiographic study. (Histochemistry 1987) · cited 218x in the literature
    "Nuclear concentration of 3H 1,25 (OH)2 vitamin D3 is also found in neurons in the periventricular nucleus of the preoptic-hypothalamic region, including its extensions, the parvocellular paraventricular and arcuate nucleus, in the ventromedial nucleus, supramammillary nucleus, reticular nucleus of the thalamus, ventral hippocampus, caudate nucleus, pallium, in the midbrain-pontine central gray, dorsal raphe nucleus, parabrachial nuclei, cranial motor nuclei, substantia gelatinosa of the sensory nucleus of the trigeminus, Golgi type II cells of the cerebellum, and others." (abstract, results, passage verified)
    pubmedfull study (doi)
0:39:22Stasha Gominaksupportedvery low

When vitamin D binds its nuclear receptor, it stimulates the expression of choline acetyltransferase, the enzyme that synthesizes acetylcholine.

"What hormones do that's unique is the hormone goes inside the nucleus of the cell and the nucleus has the DNA and it binds the DNA. And it has a special vitamin D receptor. That's what Walter was measuring. When it hits that receptor, there's a specific protein that that DNA expresses. That means that little piece of DNA comes out, it makes this protein. The protein that it makes is an enzyme that makes acetylcholine. So, that means I can trace through the scientific literature all the way from the receptor to the articles that showed that it was an enzyme called choline acetyltransferase." (said at 0:39:22)

Experimental animal research supports the claim that active vitamin D (1,25-dihydroxyvitamin D3) acting on brain regions with vitamin D receptors stimulates or upregulates the activity and expression of choline acetyltransferase (ChAT/CAT), the rate-limiting enzyme responsible for acetylcholine synthesis. Because the direct mechanistic and functional evidence comes from animal and preclinical studies, certainty is graded as very low.

0:42:53Stasha Gominaksupportedmoderate

Severe sunburns that lead to skin peeling cause skin aging even in children as young as 10 years old.

"Every sunburn that's a bad sunburn that you peel from will age your skin, even if you're 10." (said at 0:42:53)

Ultraviolet radiation causing severe, blistering/peeling sunburns initiates cumulative cellular and structural photodamage (photoaging and elastosis) that begins early in life. Dermatological literature establishes that childhood is a particularly vulnerable window for UV-induced damage, and that inadequate sun protection and severe burns in children initiate the cascade leading to premature skin aging and photocarcinogenesis.

0:43:51Stasha Gominaksupportedhigh

UVB is the specific solar wavelength of energy that triggers vitamin D synthesis in the skin.

"UVB is the wavelength that makes D." (said at 0:43:51)

The speaker's statement is fully supported. Cutaneous synthesis of vitamin D3 occurs when 7-dehydrocholesterol in the skin absorbs solar ultraviolet B (UVB) radiation (specifically in the ~290–315 nm range) and is converted into previtamin D3, which then thermally isomerizes into vitamin D3.

0:46:12Stasha Gominaksupportedhigh

Pantothenic acid is a biochemical precursor used by the body to make coenzyme A.

"It says pantothenic acid is a chemical that makes this thing called coenzyme A." (said at 0:46:12)

Pantothenic acid (vitamin B5) is the obligate biochemical precursor for the biosynthesis of coenzyme A (CoA). In mammalian cells and across living organisms, CoA is synthesized from pantothenic acid, cysteine, and ATP through a conserved five-step enzymatic pathway.

0:46:56Stasha Gominaksupportedlow

A 1950s study conducted in an Iowa prison demonstrated that blocking pantothenic acid for two weeks caused insomnia, gastrointestinal complaints and bloating, an abnormal gait, and burning sensations in the hands and feet.

"The articles that she references are from the 1950s in this creepy lab next to the Iowa State Prison where they're doing these creepy experiments on prisoners before it becomes illegal. They published this article saying, 'If you block pantothenic acid for 2 weeks, you see four things. They can't sleep. They have belly complaints, bloating and all sorts of things. They have a funny puppet-like gait and they have burning in their hands and feet.'" (said at 0:46:56)

The speaker accurately describes the classic 1950s human experimental deficiency studies conducted by Dr. William B. Bean, Dr. Robert E. Hodges, and colleagues at the State University of Iowa College of Medicine and the Iowa State Penitentiary. In these studies, healthy prisoner volunteers were administered the pantothenic acid antagonist omega-methylpantothenic acid (along with a deficient diet) to block pantothenic acid metabolism. The subjects rapidly developed characteristic deficiency manifestations, including insomnia, personality/mood changes, severe gastrointestinal disturbances (nausea, epigastric distress, abdominal cramps, flatus/bloating), neurological signs including unsteady 'steppage' or abnormal gait, and paresthesias marked by numbness and burning sensations in the hands and feet.

0:48:27Stasha Gominaksupportedlow

Blocking or being deficient in vitamin B5 (pantothenic acid) causes insomnia.

"If you block B5, you get insomnia." (said at 0:48:27)

Classic human experimental studies inducing pantothenic acid (vitamin B5) deficiency—specifically using the metabolic antagonist omega-methylpantothenic acid and/or pantothenic acid-deficient diets (dating back to the 1950s work by Bean, Hodges, et al.)—documented clinical manifestations including insomnia, fatigue, headache, paresthesias ('burning feet syndrome'), and gastrointestinal disturbances. Modern reviews of vitamin B5 biology similarly recognize insomnia as an established feature of induced pantothenic acid deficiency. Evidence is graded low certainty due to reliance on small historical experimental deficiency cohorts and narrative reviews.

1:01:45Stasha Gominaksupportedhigh

Fecal microbiota transplants are used successfully to treat and prevent death from Clostridium difficile (C. diff) infections.

"But as people are dying of things like Clostridium difficile, which C. diff is the way it's shortened, they're dying of C. diff infection and they're doing poop transplants and they live." (said at 1:01:45)

High-quality evidence from Cochrane systematic reviews and randomized controlled trials confirms that fecal microbiota transplantation (FMT) is highly effective at treating recurrent and refractory Clostridioides difficile (C. diff) infections, significantly outperforming standard antibiotic regimens in achieving infection resolution and preventing relapse.

0:37:15Stasha Gominaksupportedhigh

Walter Stumpf published his first scientific article documenting vitamin D localization in the brainstem in 1982.

"The first article is in 1982 about brainstem. He publishes articles about postpartum depression, about infertility, about obesity." (said at 0:37:15)

Walter Stumpf and colleagues published a landmark study in Science in 1982 demonstrating 1,25-dihydroxyvitamin D3 localization and target receptor sites in the rat brain (including forebrain, hindbrain/brainstem, and spinal cord) using autoradiography.

  • supports: Brain target sites for 1,25-dihydroxyvitamin D3. (Science (New York, N.Y.) 1982) · cited 225x in the literature
    "Autoradiographic studies with 3H-labeled 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] demonstrate, in certain neurons of rat forebrain, hindbrain, and spinal cord, a nuclear retention and concentration of radioactivity, which can be prevented by treatment with 1,25(OH)2D3, but not with 25-hydroxyvitamin D3. These results indicate the presence of brain receptors in addition to pituitary receptors for 1,25(OH)2D3" (abstract, passage verified)
    pubmedfull study (doi)
1:00:30Stasha Gominaksupportedmoderate

Medical literature generally considers dietary vitamin B5 (pantothenic acid) deficiency non-existent or exceptionally rare because it is ubiquitous in all food sources.

"All of the literature says, "B5 deficiency doesn't exist because it's in every food."" (said at 1:00:30)

Medical and nutritional literature consistently states that dietary pantothenic acid (vitamin B5) deficiency is exceptionally rare in humans because the nutrient is widely distributed across virtually all plant and animal food sources (its name itself derives from the Greek 'pantothen', meaning 'from everywhere'). Clinically recognized isolated deficiency is generally only seen in experimental settings using antagonists or severe, generalized malnutrition.

1:02:10Stasha Gominaksupportedhigh

The normal human gut microbiome is predominantly composed of four main bacterial groups or phyla.

"So there are four big groups of bacteria that is the normal human microbiome." (said at 1:02:10)

Scientific consensus widely recognizes that the healthy human gut microbiota is predominantly composed of four major bacterial phyla: Firmicutes (recently renamed Bacillota), Bacteroidetes (Bacteroidota), Actinobacteria (Actinomycetota), and Proteobacteria (Pseudomonadota), with Firmicutes and Bacteroidetes typically constituting the vast majority (over 90%) of the bacterial population.

1:04:30Stasha Gominaksupportedhigh

The gastrointestinal tract contains receptors for vitamin D.

"Walter talked about the GI tract having all sorts of receptors for vitamin D." (said at 1:04:30)

The vitamin D receptor (VDR) is abundantly expressed throughout the gastrointestinal tract, including the esophagus, stomach, small intestine, and colon, where it regulates calcium absorption, epithelial barrier integrity, and mucosal immune responses.

1:05:35Stasha Gominaksupportedmoderate

Research during the COVID-19 pandemic demonstrated that people who were vitamin D deficient had higher mortality from COVID-19.

"until 2020 when COVID came and they actually started to realize that the people who were D deficient died in COVID" (said at 1:05:35)

Extensive observational research and systematic reviews published during and after 2020 demonstrated that patients deficient in vitamin D had a significantly higher risk of severe COVID-19 disease and mortality. Meta-analyses indicate that while the observational association with increased mortality is robust, it is partially attenuated when adjusting for confounders, and interventional trials of vitamin D supplementation have shown mixed or non-significant effects on mortality.

1:06:00Stasha Gominaksupportedmoderate

Administering vitamin D changes the bacterial composition of human stool.

"Will giving vitamin D change the population? And yes, that's the answer." (said at 1:06:00)

Multiple randomized controlled trials and a 2026 systematic review of 14 RCTs confirm that vitamin D supplementation modifies the composition and relative abundance of specific bacterial taxa in the human gut microbiota (measured in stool), such as enriching Bifidobacteriaceae/Bifidobacterium and modulating specific genera, although the exact shifts vary based on baseline vitamin D status, dosage, duration, and patient population.

1:15:00Stasha Gominaksupportedlow

Lactobacillus reuteri produces a specific chemical messenger metabolite that participates in regulating iron in the body.

"And if you do not have a specific bacteria called Lactobacillus reuteri, you will be missing a brand new metabolite or chemical that was named after that bacteria just in the last 3 years that's—called reuteri that is one of the chemical messengers that our body uses." (said at 1:15:00)

A 2020 study in Cell Metabolism identified that gut microbiota-derived metabolites, including reuterin (a metabolite produced by Lactobacillus reuteri and named after the species), act as chemical messengers that suppress intestinal hypoxia-inducible factor 2α (HIF-2α) and increase ferritin, thereby regulating intestinal iron absorption and systemic iron homeostasis in preclinical models. Although reuterin itself was discovered in earlier decades, its novel role as a host signaling messenger in iron regulation was characterized recently.

1:17:05Stasha Gominaksupportedhigh

The scientific literature does not support the claim that taking vitamin D supplements causes or creates a B vitamin deficiency.

"I want to go back to Madeline. So, my question was because the research that I'm reading says that vitamin D does not cause, trigger, or create a B vitamin deficiency. GUEST1: No, it's not in the literature except my article." (said at 1:17:05)

There is no established evidence in the peer-reviewed scientific literature demonstrating that vitamin D supplementation causes, triggers, or induces a B vitamin deficiency. The notion stems almost exclusively from a single speculative hypothesis paper published in Medical Hypotheses (Gominak, 2016; PMID 27515213), which theorized an interaction between vitamin D, the gut microbiome, and pantothenic acid (vitamin B5) based on uncontrolled clinical observations. Outside of this hypothesis, standard medical literature and clinical trials do not show that taking vitamin D causes B vitamin depletion.

1:18:25Stasha Gominaksupportedmoderate

Cutaneous production rate of vitamin D decreases as humans get older.

"even though this is dogma at the moment that our production of vitamin D goes down as we get older. So, if you look back to that person who was 75, who didn't get sick until they were 75, their skin production, even though they're still out there with their truck farm and still raising their own food, their skin production rate of vitamin D goes down" (said at 1:18:25)

Published experimental and physiological evidence demonstrates that the capacity of human skin to synthesize vitamin D3 declines significantly with age. In human skin samples across age ranges from 8 to 92 years, aging was associated with a marked decrease in epidermal concentrations of the precursor 7-dehydrocholesterol and a greater than twofold reduction in previtamin D3 synthesis upon ultraviolet exposure in older individuals compared to younger individuals.

1:07:02Stasha Gominaksupportedmoderate

All eight essential B vitamins are synthesized by the human gut microbiome.

"It turns out that all the Bs come from the microbiome." (said at 1:07:02)

Genomic and metabolic pathway assessments of common human gut bacteria confirm that biosynthesis pathways for all eight essential B vitamins (thiamin [B1], riboflavin [B2], niacin [B3], pantothenic acid [B5], pyridoxine [B6], biotin [B7], folate [B9], and cobalamin [B12]) exist within the human gut microbiome. A comprehensive genomic analysis of 256 representative human gut microbial genomes found that between 40% and 65% of analyzed gut microbes possess the pathways to synthesize each of the eight B vitamins, with extensive microbial sharing and cross-feeding. While gut microbial synthesis contributes to local intestinal and host micronutrient pools, dietary intake remains necessary to fully satisfy host metabolic requirements.

1:35:07Stasha Gominaksupportedmoderate

Melanin absorbs energy to protect skin DNA from sun damage, and genetic variants associated with red hair evolved in northern latitudes to allow people to synthesize vitamin D by reducing melanin-mediated UV blockage.

"So, melanin is the pigment that humans have in their skin. You have more than I do. I put more melanin as I stay out in the sun more and I tan. That melanin is absorbing energy. It's there to protect you from overexposure to sunlight and damaging effects on the DNA of your skin. The redhead gene usually comes with freckles, which means that there is only little tiny parts of the skin that have melanin. And the redhead gene came about in the far north, Viking Scotland. And those places don't get much sunlight. That means it cleared out the blocker of the thing that collected that energy and allowed people who lived in very overcast environments to make D because the melanin didn't block the conversion to vitamin D and all these other things that it does." (said at 1:35:07)

The speaker accurately describes the dual evolutionary model of human skin pigmentation (the vitamin D–folate hypothesis). Melanin acts as an optical filter and broad-spectrum photoprotectant that absorbs ultraviolet radiation (UVR) to shield dermal DNA and folate from UV-induced damage. As ancestral human populations migrated into high-latitude, low-UVB regions (such as northern Europe), selective pressures favoured depigmented skin phenotypes—including loss-of-function variants in the melanocortin 1 receptor (MC1R) gene that produce red hair, fair skin, and freckles—to facilitate UVB penetration for sufficient cutaneous synthesis of vitamin D3.

1:38:57Stasha Gominaksupportedhigh

Coenzyme A is biochemically required for the synthesis of acetylcholine, cortisol, and melatonin.

"It makes acetylcholine which allows our whole autonomic nervous system to sleep nor—to react normally. So, it affects all of those things that we do when we're training and it also affects cortisol levels. You must have coenzyme A to make cortisol. You must have coenzyme A to make melatonin." (said at 1:38:57)

Coenzyme A (as acetyl-CoA) is an obligatory biochemical substrate/precursor for the synthesis of acetylcholine, melatonin, and steroid hormones including cortisol: (1) Acetylcholine is synthesized from choline and acetyl-CoA by choline acetyltransferase (ChAT); (2) Melatonin synthesis requires acetyl-CoA in the rate-limiting conversion of serotonin to N-acetylserotonin by arylalkylamine N-acetyltransferase (AANAT); (3) Cortisol is synthesized from cholesterol, whose de novo biosynthetic backbone is derived entirely from acetyl-CoA.

1:39:51Stasha Gominaksupportedhigh

UVA radiation tans the skin but does not produce vitamin D.

"And it's important that UVA, if you're going to go to a tanning salon, if they're using UVA, you are not making vitamin D from that. So, there are different kinds of beds. UVA will still tan you, but it will not make D." (said at 1:39:51)

Cutaneous synthesis of vitamin D3 occurs when 7-dehydrocholesterol absorbs ultraviolet B (UVB) radiation (approximately 280–315 nm). In contrast, ultraviolet A (UVA) radiation (315/320–400 nm) induces melanogenesis (skin pigmentation/tanning) but lacks the photon energy necessary to convert 7-dehydrocholesterol into previtamin D3. Randomized testing in commercial tanning beds has demonstrated that tanning beds emitting UVB stimulate cholecalciferol and 25-hydroxyvitamin D synthesis, whereas control tanning beds without UVB (emitting UVA) do not produce vitamin D.

  • supports: Changes in serum 25-hydroxyvitamin D and cholecalciferol after one whole-body exposure in … (Endocrine 2012) · cited 8x in the literature
    "Healthy volunteers were randomized to one whole-body exposure in a commercial tanning bed with UVB emission (UVB/UVA ratio 1.8-2.0%) or an identical placebo tanning bed without UVB. The output in the 280-320 nm range was 450 µW/cm². Blood samples were analyzed for 25OHD and cholecalciferol at baseline and during 7 days after treatment... At the end of the study, we found a mean increase of 25OHD in the UVB group of 4.5 nmol/l (SD 7 nmol/l) compared to a decline of -1.2 nmol/l (SD 7 nmol/l) in the placebo group (p = 0.1). A linear mixed model yielded an increase of 25OHD in the UVB group of 1.0 nmol/l per 24 h (p < 0.01)." (abstract, results, passage verified)
    pubmedfull study (doi)
1:40:20Stasha Gominaksupportedhigh

Standard window glass prevents the skin from producing vitamin D.

"No, you can't make anything through the window." (said at 1:40:20)

Standard window glass absorbs/blocks virtually all solar ultraviolet B (UVB) radiation (wavelengths ~290–315 nm), which is the specific portion of the solar spectrum required for the photolysis of 7-dehydrocholesterol to previtamin D3 in human skin. Experimental and physiological data confirm that sunlight exposure through standard glass fails to increase circulating levels of 25-hydroxyvitamin D.

1:40:41Steven Bartlett (host)supportedmoderate

Up to 80% of UV radiation penetrates light cloud cover, whereas thick, dense storm clouds can block 70% to 90% of UVB rays.

"up to 80% of UV radiation still penetrates light cloud cover, so you can absolutely still make vitamin D, though it might take a few minutes longer than it would on a completely clear day. When it's thick, dark, and overcast uh or dense storms or clouds, that can block up to 70 to 90% of UVB rays." (said at 1:40:41)

Atmospheric and photobiological measurements support the claim. Widely accepted public health and meteorological data (e.g., from the World Health Organization and EPA) establish that up to 80% of solar UV radiation penetrates light cloud cover, allowing cutaneous vitamin D synthesis to continue with modestly increased exposure times. Empirical measurements of vitamin D effective UV radiation (UVD3) demonstrate transmission ratios around 71% under high partial cloud cover (6.5-7.5 octas), while thick, overcast, or dense storm clouds attenuate the majority of UVB irradiance (blocking 70% to >90%).

1:41:28Stasha Gominaksupportedmoderate

Infrared light penetrates human tissue several centimeters and provides energy to mitochondria.

"And infrared is one of the most important uh wavelengths that we know about that penetrates the body several centimeters and actually gives energy to the mitochondria." (said at 1:41:28)

Near-infrared (NIR) light in the optical therapeutic window penetrates human tissue deeper than visible light (typically several millimeters to several centimeters depending on tissue density, skull/scalp thickness, and laser/LED parameters). The established primary mechanism of photobiomodulation (PBM) involves photon absorption by mitochondrial chromophores—predominantly cytochrome c oxidase (complex IV of the respiratory chain)—which enhances electron transport, ATP synthesis, and cellular energy metabolism.

1:46:10Stasha Gominaksupportedhigh

Beriberi is a disease associated with a pure carbohydrate/polished rice diet that presents with heart failure, non-healing leg ulcers, bright shiny red skin, and burning in the feet.

"One of them was in the Japanese prisoner of war camps and the Bataan Death March in World War II where they had rice, rice, rice. That's it. And they're outside all the time. They're not vitamin D deficient. They're discovered to have beriberi and beriberi is an old disease described in Japan when you take off the rice casing. So, ultimately they gave back meat and vegetables and beriberi is described as heart failure, non-healing ulcers of the legs, bright shiny red skin and burning in the feet that we see in the elderly in the US all the time in the hospital." (said at 1:46:10)

Beriberi is a nutritional deficiency disease caused by lack of thiamine (vitamin B1), historically associated with polished white rice diets (due to the removal of the thiamine-rich outer husk). It presents clinically in two primary forms: 'wet beriberi', characterized by high-output congestive heart failure and extensive peripheral edema (which often causes shiny, stretched, erythematous skin and ulcerations), and 'dry beriberi', characterized by peripheral neuropathy presenting with paresthesias and burning sensations in the lower extremities ('burning feet'). These manifestations were extensively documented in Far Eastern prisoner-of-war camps during WWII where prisoners subsisted almost entirely on polished white rice.

1:55:27Stasha Gominaksupportedmoderate

Vitamin D has specific receptors in the brainstem.

"But, it's also true that vitamin D has receptors in the brainstem." (said at 1:55:27)

Published neuroanatomical studies in both human post-mortem brain tissue and rodent models demonstrate that vitamin D receptors (VDR) are expressed in the brainstem, including prominent nuclear localization in the substantia nigra (midbrain) and other brainstem regions.

1:33:39Stasha Gominaksupportedhigh

Fermenting bacteria in fermented foods produce and secrete B vitamins.

"bacteria are growing in here and they're secreting things like B vitamins and reuteri. They're making a yeast bacterial mixture... You're basically eating a food that has B50 in it." (said at 1:33:39)

It is well-established that various fermenting microorganisms, including lactic acid bacteria (such as Limosilactobacillus reuteri, Lactiplantibacillus plantarum, and Leuconostoc species) and yeasts, synthesize and secrete B vitamins (including riboflavin [B2], niacin/NMN [B3], folate [B9], and cobalamin [B12]) during the fermentation of foods and culture media.

4 No source found (not proven false)
1:32:14Stasha Gominakunverifiedvery low

Vitamin D synthesized naturally in the skin is sulfated, unlike supplemental vitamin D.

"There is a lot of literature by a gal named Stephanie Seneff who says that the vitamin D that we make on our skin is sulfated, which is different than the vitamin D we're taking as supplement." (said at 1:32:14)

Established biochemistry and photobiology demonstrate that cutaneous vitamin D synthesis occurs via UVB-induced photolysis of 7-dehydrocholesterol to previtamin D3, which thermally isomerizes into cholecalciferol (vitamin D3)—chemically identical to supplemental cholecalciferol. While computer scientist Stephanie Seneff has published speculative, non-empirical hypotheses proposing that cutaneous synthesis produces vitamin D sulfate, no validated scientific literature or experimental evidence demonstrates that natural skin synthesis produces sulfated vitamin D or that it differs chemically from standard supplemental vitamin D3.

1:11:12Stasha Gominakunverifiedvery low

In a clinical case, a patient (Madeline) taking 30,000 IU of vitamin D daily for 4 years maintained serum 25-hydroxyvitamin D levels in the 60s ng/mL while experiencing resolution of extremity neuropathy pain and depression.

"Madeline is struggling with all these things. She's slowly getting better. Then we do the D, she's slowly getting better. Then we do the B100. And then it's freaking awesome. She starts to lose the pain that she had down her leg. The burning in her hands and feet goes away. Her sleep gets much better. Now, she's into year three and four of what becomes the RightSleep program. And she's still on 30,000 IUs of D a day... Her D level has stayed the same. It's in the 60s... Her depression is gone. She's stopped three medicines that we've been using for pain control." (said at 1:11:12)

No published case report or formal clinical trial documenting the specific patient case ('Madeline') taking 30,000 IU/day of vitamin D for 4 years with resolution of neuropathy pain and depression could be located in PubMed or Europe PMC. The clinician (Dr. Stasha Gominak) has published theoretical hypothesis papers in Medical Hypotheses describing uncontrolled clinical observations of vitamin D (targeting serum levels of 60-80 ng/mL) and B-complex supplementation in patients with neurologic and sleep disorders, but the specific patient narrative is an unpublished clinical anecdote.

1:20:43Steven Bartlett (host)unverifiedvery low

Excessive doses of supplemental B vitamins can cause sleep disruption and pain once the intestinal microbiome has normalized.

"Both sleep disruption and pain can be caused by large doses of B vitamins once the intestinal microbiome has returned to normal." (said at 1:20:43)

The claim originates from a speculative clinical hypothesis by Dr. Stasha Gominak published in the journal Medical Hypotheses (PMID 27515213), based on uncontrolled observations in neurology patients given vitamin D and B-complex supplements (B100). The paper hypothesizes relationships between vitamin D, gut bacterial B-vitamin synthesis, sleep regulation, and pain pathways. However, there are no published controlled trials or rigorous mechanistic studies establishing that excessive B-vitamin supplementation causes sleep disruption or pain specifically secondary to the normalization of the intestinal microbiome.

1:37:14Steven Bartlett (host)unverifiedvery low

According to USA Today, 90% of Americans spend close to 22 hours inside daily, and roughly 20% never go outside, regularly spending 24 hours indoors.

"There's some interesting stats I found which says that 90% of Americans spend close to 22 hours inside every day. That was from USA Today. And roughly 20% of Americans never go outside, regularly spending 24 hours indoors." (said at 1:37:14)

No matching publication or survey data could be retrieved from the database to confirm the exact figures cited from USA Today (that 90% of Americans spend close to 22 hours inside daily and roughly 20% never go outside / spend 24 hours indoors). While widely publicized figures from sources such as the National Human Activity Pattern Survey (NHAPS) indicate Americans spend on average roughly 87% of their time in enclosed buildings and 6% in vehicles (~22 hours total inside), the specific statistical breakdown stated by the host could not be verified in the retrieved scientific literature.

Unverified means no publication matching the claim was located; it does not prove the claim false. Spotted an error? See the corrections policy - disputes from the people quoted are prioritized.