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

56 research-tied claims examined: 11 contradicted 1 overstated 5 context 35 supported 4 unverified

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.

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.