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

11 Contradicted by research
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.

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.