HoldsUp

FoundMyFitness · 2016-04-09 · Rhonda Patrick (host), Dominic D'Agostino

Dominic D'Agostino, Ph.D. on Modified Atkins Diet, Keto-Adaptation, Ketosis & More

56 claims checked against research: 2 contradicted 3 overstated 5 needing context 39 supported 7 unverified

2

Contradicted by research

0:47:01Dominic D'Agostinocontradictedlow

Fasting and ketogenic diets increase the permeability of the blood-brain barrier to various compounds and drugs.

"We know with fasting and the ketogenic diet that you can increase permeability to the blood-brain barrier, things get through faster... Fasting-induced ketosis or even the ketogenic diet help increase the permeability of the blood-brain barrier to a wide variety of things. So if you are—sort of the implications from his perspective that if you're getting a chemotherapeutic drug, if you're getting some kind of drug that needs to cross the blood-brain barrier that's impaired in some way, you might be able to get that across faster in a state of fasting ketosis or the ketogenic diet." (said at 0:47:01)

Fasting and ketogenic diets do not cause a generalized increase in blood-brain barrier (BBB) permeability to a wide variety of compounds or chemotherapeutic drugs. While fasting and ketosis induce selective upregulation of specific nutrient transporters—most notably monocarboxylate transporter 1 (MCT1) to facilitate ketone body uptake into the brain—preclinical research demonstrates that fasting does not alter major drug efflux transporters (such as P-glycoprotein) or induce broad BBB permeability. Furthermore, ketogenic and fasting interventions are generally associated with preserving or restoring BBB integrity and tight junction function rather than making the barrier more permeable.

1:36:35Dominic D'Agostinocontradictedmoderate

Being on a ketogenic diet reduces circulating blood glutamine levels.

"I think that will lower your your blood glutamine levels. Just being on a ketogenic diet will do that" (said at 1:36:35)

Published clinical and preclinical evidence does not support the claim that following a ketogenic diet reduces circulating blood glutamine levels. Randomized clinical trials evaluating the impact of ketogenic diets on systemic amino acid profiles demonstrate significant reductions in specific amino acids (such as alanine, methionine, threonine, and tryptophan) and elevations in branched-chain amino acids, but circulating glutamine levels are tightly regulated and not systematically reduced by ketosis. Furthermore, metabolic cancer research exploring dual fuel restriction has demonstrated that while a ketogenic diet lowers circulating glucose, it does not deplete systemic glutamine, which requires pharmacological glutamine antagonists (such as DON or CB-839) to target.

3

Overstated

0:31:42Dominic D'Agostinooverstatedvery low

Shifting toward oxidative phosphorylation and ketone metabolism forces cells to upregulate mitochondrial biogenesis and electron transport chain proteins.

"In the context of, yeah, any kind of cell, like or tissue really, skeletal muscle or cancer cell, yeah, you are forcing the body in a way, and it's a stress initially, to upregulate mitochondrial machinery, really, and more mitochondria. Mitochondria will start, you know, budding off and creating mitochondrial biogenesis... Then the proteins that are associated with the electron transport chain, those proteins are upregulated, so you make more of these proteins." (said at 0:31:42)

While ketone supplementation and ketogenic diets have been shown to stimulate mitochondrial biogenesis and upregulate electron transport chain proteins in specific animal tissues, claiming this occurs universally across 'any kind of cell... skeletal muscle or cancer cell' overstates the published evidence. In male mice fed a ketone ester diet, electron transport chain proteins and mitochondrial biogenesis-regulating proteins doubled in interscapular brown adipose tissue (PMID: 22362892). Similarly, a ketogenic diet induced mitochondrial biogenesis in a mouse model of mitochondrial myopathy (PMID: 20167576). However, these findings are restricted to preclinical rodent models and specific tissue contexts rather than human trials or universal cell types.

0:48:47Dominic D'Agostinooverstatedvery low

PET imaging of neuroinflammation in the brain can predict the occurrence of epileptic seizures.

"So there's this PET scan technique that allows us to look at neuroinflammation in the brain. [0:48:47] HOST: Yeah. [0:48:47] GUEST1: And we know that—this is a conference that I recently came from—that may be an excellent predictor of when someone's going to have a seizure." (said at 0:48:47)

Preclinical animal models have shown that positron emission tomography (PET) imaging of neuroinflammation—specifically targeting the 18 kDa translocator protein (TSPO) as a marker of microglial activation—can predict epileptogenesis and seizure burden in rodent models of temporal lobe epilepsy. In humans, TSPO PET is used to help locate focal epileptic lesions and correlate neuroinflammation with seizure severity. However, using PET imaging to predict the specific occurrence or timing of epileptic seizures in humans is not an established clinical tool and remains predominantly in the preclinical research stage.

1:34:10Rhonda Patrick (host)overstatedmoderate

When ingested orally, the gut and liver consume the vast majority of glutamine, resulting in very little entering the bloodstream.

"when you take glutamine orally, the gut takes it, it's not entering your bloodstream, it's not being, you know, so the gut and the liver take take its share, and very little of it actually gets into the bloodstream." (said at 1:34:10)

Human stable isotope tracer studies show that the splanchnic bed (gut and liver) extracts a substantial proportion—approximately 50% to 75%—of orally/enterally administered glutamine during first-pass metabolism, primarily through intestinal mucosal oxidation. However, the claim that "very little of it actually gets into the bloodstream" or that "it's not entering your bloodstream" is overstated. Between 25% and 50% of ingested glutamine escapes splanchnic extraction and enters systemic circulation, leading to substantial, dose-dependent increases in plasma glutamine concentrations.

5

Needs context

0:16:51Rhonda Patrick (host)needs contextvery low

Bile acids such as deoxycholic acid released during fat digestion cause endotoxin release.

"fat itself, in order to be digested, you have to make these bile acids like deoxycholic acid, which causes endotoxin release." (said at 0:16:51)

The statement conflates normal human bile synthesis with bacterial bile metabolism and the mechanism of endotoxin translocation. Primary bile acids (such as cholic acid and chenodeoxycholic acid) are synthesized by the liver to aid lipid digestion. Deoxycholic acid (DCA) is not produced directly by the human host for digestion; rather, it is a secondary bile acid formed in the intestine through the modification of primary bile acids by colonic bacteria. In vitro models demonstrate that secondary bile acids such as DCA can impair intestinal epithelial barrier integrity and increase paracellular permeability, which is a recognized pathway facilitating the translocation of bacterial endotoxin (lipopolysaccharide) across the gut barrier. However, bile acids do not directly generate or release endotoxins.

0:30:40Dominic D'Agostinoneeds contextlow

Using ketones as a metabolic fuel increases mitochondrial efficiency, requiring less oxygen to generate the same amount of ATP and producing fewer reactive oxygen species.

"From an acute point of view, as simply as a metabolic fuel, the mitochondrial efficiency is greater, so you'll have a greater mitochondrial membrane potential, a greater driving force for ATP synthase to make ATP. So it energizes the mitochondria in a way that would be expected from a metabolic fuel that's sort of superior from a bioenergetic point of view. So you have a greater capacity to generate ATP for a given amount of oxygen that's available. So with that occurring, the metabolic efficiency of the cell would be sort of preserved. You're using less oxygen to make the same amount of ATP, less reactive oxygen species." (said at 0:30:40)

The claim that ketone bodies increase ATP production and lower reactive oxygen species (ROS) levels is supported under certain stress conditions in cellular and animal models (PMID 25649993, PMID 12975474). For example, D-beta-hydroxybutyrate stimulates ATP production and reduces ROS levels in glucose-deprived cortical cultures (PMID 25649993). However, the generalization that ketone utilization inherently increases mitochondrial efficiency, uses less oxygen for a given ATP yield, and always reduces ROS is contradicted by other metabolic evidence. In healthy cortical neurons, ketone metabolism increases oxygen consumption and stimulates gene expression through the deliberate generation of ROS (PMID 27739595). Additionally, in vivo animal models of whole-body ketosis demonstrate a moderate uncoupling state resulting in lower oxidative efficiency compared to glucose oxidation (PMID 23852511).

0:33:36Rhonda Patrick (host)needs contextmoderate

Under normal physiology, astrocytes metabolize glucose and shuttle lactate to neurons, which convert lactate into pyruvate as an energy source.

"So neurons themselves actually use lactate generated from astrocytes. So they're using—I mean, neurons are actually using lactate, it's an energetically favorable source of energy, much like ketones... the astrocytes are using glucose, and that's why the brain uses glucose, and they're producing the lactate. The neurons are using the lactate because it's, you know, getting shunted and converted into pyruvate." (said at 0:33:36)

The speaker is describing the Astrocyte-Neuron Lactate Shuttle (ANLS) hypothesis, first proposed by Pellerin and Magistretti in 1994. Under this model, astrocytes take up glucose, perform glycolysis, and export lactate via monocarboxylate transporters, which neurons import and convert back to pyruvate via lactate dehydrogenase (LDH) for oxidative metabolism. While substantial mechanistic, animal, and in vitro evidence demonstrates that neurons can oxidize astrocyte-derived lactate—particularly during periods of synaptic plasticity or metabolic stress—the ANLS remains a debated model rather than an absolute rule of baseline brain metabolism. Neurons possess their own glucose transporters and glycolytic machinery, and direct neuronal glucose utilization is well-established as essential for sustaining synaptic transmission.

1:24:30Dominic D'Agostinoneeds contextvery low

Metformin causes mitochondrial stress by inhibiting complex I or complex II of the electron transport chain.

"And interestingly, metformin causes uh mitochondrial stress and actually mitochondrial uh damage, some researchers coined the term, you know, that it's it's it's stimulating reactive oxygen species production uh and causing mitochondrial dysfunction, metformin is, and this is kind of well known in the field... a lot of people are studying it from the perspective of, you know, impaired complex I or complex II activity in the mitochondria" (said at 1:24:30)

Metformin is well established in biochemical and cellular studies to inhibit respiratory chain complex I (NADH:ubiquinone oxidoreductase), leading to mild mitochondrial respiratory suppression, altered cellular energy balance, and AMPK activation. However, metformin selectively targets complex I and does not inhibit complex II; succinate-driven respiration through complex II remains functional and is frequently used experimentally to bypass metformin-induced complex I inhibition.

1:41:40Dominic D'Agostinoneeds contextlow

Exogenous ketone ester supplementation was originally investigated and developed for preventing central nervous system oxygen toxicity.

"And for oxygen toxicity, obviously, that was the original application." (said at 1:41:40)

Exogenous ketone esters, specifically 1,3-butanediol acetoacetate diester (BD-AcAc2) and (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, have been investigated for delaying central nervous system oxygen toxicity (CNS-OT) seizures in hyperbaric oxygen environments, with preclinical studies demonstrating significant delays in seizure latency. However, while CNS oxygen toxicity prevention (for military divers and hyperbaric oxygen applications) has been a primary target of research funding and preclinical evaluation (e.g., ONR-funded work by D'Agostino et al.), exogenous ketone esters were originally conceptualized and synthesized by Richard Veech, Kieran Clarke, and colleagues primarily as a metabolic tool to improve physical and cognitive performance, cardiac efficiency, and physical endurance under physiological stress. Thus, while preventing CNS oxygen toxicity was a early and prominent application investigated in preclinical models, framing it as the single original application requires qualification.

39

Supported by research

0:03:58Dominic D'Agostinosupportedhigh

Suppression of the hormone insulin drives hepatic ketogenesis.

"the suppression of the hormone insulin drives hepatic ketogenesis; it drives the body's ability to make ketones" (said at 0:03:58)

Established metabolic physiology confirms that hepatic ketogenesis is driven by low insulin concentrations (or an increased glucagon-to-insulin ratio). A decline or suppression in circulating insulin disinhibits peripheral lipolysis in adipose tissue, increasing free fatty acid delivery to the liver. Within hepatocytes, low insulin levels and glucagon signaling reduce malonyl-CoA, relieving the inhibition of carnitine palmitoyltransferase I (CPT-1), which allows fatty acid entry into the mitochondria for beta-oxidation and ketone body production.

  • supports: Energy metabolism in the liver. (Comprehensive Physiology 2014) · cited 1995x in the literature
    "In the fasted state, the liver secretes glucose through both glycogenolysis and gluconeogenesis... Fasting also promotes lipolysis in adipose tissue, resulting in release of nonesterified fatty acids which are converted into ketone bodies in hepatic mitochondria though β-oxidation and ketogenesis." (abstract)
    pubmedfull study (doi)
  • supports: The regulation of ketogenesis. (Ciba Foundation symposium 1982) · cited 38x in the literature
    "Insulin deficiency triggers the lipolytic process in adipose tissue with the result that free fatty acids pass into the plasma for uptake by liver and other tissues. Glucagon appears to be the primary hormone involved in the induction of fatty acid oxidation and ketogenesis in the liver... Administration of food after a fast, or of insulin to the diabetic subject, reduces plasma free fatty acid concentrations, increases the liver concentration of malonyl-CoA, inhibits carnitine acyltransferase I and reverses the ketogenic process." (abstract, passage verified)
    pubmedfull study (doi)
0:06:06Rhonda Patrick (host)supportedvery low

Beta-hydroxybutyrate acts as a signaling molecule that turns on genes involved in stress resistance and longevity, including FOXO3.

"it's able to turn on genes that are involved in dealing with stress better. Some of these genes are involved in longevity: FOXO3 for one." (said at 0:06:06)

Preclinical evidence demonstrates that beta-hydroxybutyrate (βOHB) functions as an epigenetic signaling molecule by inhibiting class I histone deacetylases (HDACs). In cell culture and mouse models, this HDAC inhibition increases histone acetylation at the promoters of oxidative stress resistance and longevity-related genes, specifically activating Foxo3a (FOXO3) and Mt2, which protects tissues against oxidative stress. Because these findings are established in cellular and animal models without direct human trial confirmation, the body of evidence is rated very low certainty.

0:09:11Dominic D'Agostinosupportedhigh

The classical ketogenic diet used for drug-resistant epilepsy consists of approximately 85% to 90% fat and 8% to 10% protein.

"the ketogenic diet, as it is used classically for drug-resistant epilepsy, the original was like 90% fat—like 85% to 90% fat and maybe about 10% protein typically, 8% to 10% protein, and very minimal amount of carbohydrate." (said at 0:09:11)

The classical ketogenic diet historically developed and clinically used for drug-resistant (refractory) epilepsy is formulated based on a fat-to-(carbohydrate plus protein) weight ratio, typically 3:1 to 4:1. Because fat provides 9 kcal/g while carbohydrate and protein provide 4 kcal/g, a standard 4:1 ratio corresponds to 90% of total energy from fat and 10% from protein and carbohydrates combined (with 3:1 yielding approximately 87% fat). Protein is typically restricted to 8% to 10% of daily caloric intake to satisfy minimum physiological requirements while minimizing gluconeogenesis, with minimal carbohydrate intake.

0:10:45Dominic D'Agostinosupportedmoderate

Studies indicate the classical ketogenic diet can elevate LDL and cause high triglyceride levels in children.

"There's a few studies showing that it can influence a lipid profile in a negative way, meaning high elevation of LDL. And in kids, I think, that follow the diet, they had a high level of triglycerides. There was one study that's often referenced in regard to the ketogenic diet being atherogenic; the triglycerides are really high in some of the kids." (said at 0:10:45)

Multiple prospective studies and reviews in children treated with the classical ketogenic diet (typically for drug-resistant epilepsy) demonstrate substantial increases in serum low-density lipoprotein (LDL) cholesterol and triglycerides, frequently resulting in an atherogenic dyslipidemia profile during treatment.

0:13:38Dominic D'Agostinosupportedmoderate

Published work by Eric Kossoff shows that the modified Atkins diet has comparable therapeutic potency to the strict classical 4:1 ketogenic diet.

"So some work that Eric Kossoff has been doing over the years and publishing on is showing that the modified Atkins diet has much of the therapeutic potency of the strict classical 4:1 ketogenic diet." (said at 0:13:38)

Dr. Eric Kossoff pioneered the modified Atkins diet (MAD) for refractory epilepsy at Johns Hopkins beginning in 2003. In multiple published prospective studies, retrospective series, and 10-year review analyses, Kossoff and colleagues reported that the modified Atkins diet achieves rates of seizure reduction (e.g., approximately 45–50% achieving ≥50% reduction and ~30% achieving ≥90% reduction) comparable to those historically seen with the strict 4:1 classical ketogenic diet, with better tolerability and fewer dietary restrictions.

0:14:03Dominic D'Agostinosupportedhigh

The modified Atkins diet consists of approximately 65% to 70% fat, 20% to 30% protein, and no more than 5% to 10% carbohydrates.

"instead of 90% fat, the modified Atkins diet is roughly 65% to maybe 70% fat, which is kind of what I follow now, and about 20% to 30% protein, with the balance being still very low in carbohydrates, like no more than 5% or 10% carbohydrates." (said at 0:14:03)

The modified Atkins diet (MAD) is an established variant of ketogenic dietary therapy originally designed as a less restrictive alternative to the classic 4:1 ketogenic diet. In standard clinical protocols, the classic ketogenic diet provides approximately 90% of total calories from fat, whereas the modified Atkins diet typically targets roughly 60% to 70% of calories from fat, 20% to 30% from protein, and 5% to 10% from carbohydrates (typically capped at 10 to 20 grams of net carbohydrates per day). The speaker's breakdown accurately reflects the standard macronutrient composition defined in ketogenic diet literature.

0:29:40Dominic D'Agostinosupportedvery low

Oxidation of ubiquinone (Q) during beta-hydroxybutyrate metabolism reduces the electron availability to react with oxygen, decreasing superoxide anion and ROS generation.

"so ubiquinone, if ubiquinone is oxidized, which is achieved with our beta-hydroxybutyrate metabolism, if that's oxidized, then you have less availability for that electron to react with molecular oxygen in the metabolic pathway, so you would produce less superoxide anion, which is your precursor to more reactive oxygen species." (said at 0:29:40)

The speaker accurately describes the classic thermodynamic and biochemical mechanism established by Veech and colleagues regarding ketone body metabolism. Metabolism of beta-hydroxybutyrate reduces the mitochondrial NAD+/NADH couple while oxidizing the mitochondrial coenzyme Q (ubiquinone) pool. Because ubiquinone is maintained in a more oxidized state, the pool of reduced semiquinone intermediates available to non-enzymatically donate single electrons to molecular oxygen is diminished, leading to reduced generation of superoxide anions and downstream reactive oxygen species (ROS). Because evidence for this specific mitochondrial mechanism derives primarily from isolated mitochondrial models, animal tissue preparations, and biochemical reviews, the certainty of evidence is graded as very low.

0:30:02Dominic D'Agostinosupportedvery low

Langendorff perfused heart preparations show that the heart has greater hydraulic efficiency and generates proportionately more ATP per oxygen consumed in the presence of ketones.

"And that's been shown elegantly in a number of models, including the cardiac model which he did, the Langendorff model, the perfused heart preparation, showing that you get a greater hydraulic efficiency of the heart in the presence of ketones. You know, with a given amount of oxygen, you can generate proportionately more ATP energy currency." (said at 0:30:02)

Classic ex vivo working perfused rodent heart studies, such as those conducted by Richard Veech's laboratory, demonstrated that adding a physiological ratio of ketone bodies (D-beta-hydroxybutyrate and acetoacetate) to glucose perfusate improved cardiac hydraulic efficiency (hydraulic work per oxygen consumed) by approximately 25% to 35% and increased the free energy available from ATP hydrolysis. Because this evidence is derived from ex vivo animal tissue preparations, the overall certainty is graded as very low.

0:29:01Dominic D'Agostinosupportedlow

Initiating a ketogenic diet acts as a physiological stressor that activates the Nrf2 signaling pathway.

"That's increased initially. So yeah, it actually activates like Nrf2 and stuff, so when someone gets on a ketogenic diet, there's—it's a stress to the body." (said at 0:29:01)

Preclinical and mechanistic evidence supports the concept that adopting a ketogenic diet and metabolizing ketone bodies (such as beta-hydroxybutyrate) acts as a mild physiological/mitochondrial stressor (hormesis), which triggers the activation of the master antioxidant transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2). This activation subsequently upregulates endogenous antioxidant and cytoprotective defenses. The available evidence comes primarily from animal models, cell culture experiments, and mechanistic reviews rather than human clinical trials, resulting in a low GRADE certainty.

0:32:22Dominic D'Agostinosupportedhigh

Ketones and lactate are transported across cell membranes via monocarboxylate transporters (MCTs).

"HOST: It goes through the same transporter, right? GUEST1: Yeah, MCT." (said at 0:32:22)

Both ketone bodies (such as acetoacetate and beta-hydroxybutyrate) and lactate are monocarboxylates transported across cellular membranes (including at the blood-brain barrier) by proton-coupled monocarboxylate transporters (MCTs 1–4, encoded by the SLC16 gene family).

0:35:50Dominic D'Agostinosupportedmoderate

Internalization or impairment of neuronal GLUT3 glucose transporters is linked to Alzheimer's disease pathology.

"Well, there's a whole host of reasons or things that can cause impaired brain energy, brain glucose metabolism, and that could be internalization of the GLUT3 transporter, which occurs—it's kind of linked to Alzheimer's pathology... Primarily in neurons." (said at 0:35:50)

Published post-mortem human brain studies and animal models demonstrate that impairment, reduction, and altered membrane trafficking/translocation of the neuronal glucose transporter GLUT3 in cortical and hippocampal regions are closely linked to Alzheimer's disease pathology (such as amyloid-beta accumulation) and associated cerebral hypometabolism.

0:36:11Dominic D'Agostinosupportedmoderate

Pyruvate dehydrogenase complex activity is deficient in neurodegenerative conditions such as Alzheimer's disease.

"And there's a couple of key enzymes that are either deficient or not active like they should be. Pyruvate dehydrogenase complex is deficient." (said at 0:36:11)

Multiple postmortem biochemical and proteomic studies in humans have demonstrated that the activity and protein levels of the pyruvate dehydrogenase complex (PDHC) are significantly reduced in the brains of individuals with Alzheimer's disease and other neurodegenerative disorders (such as Huntington's disease) compared to controls.

0:38:40Dominic D'Agostinosupportedvery low

A ketogenic diet increases the brain GABA to glutamate ratio, partly by upregulating glutamic acid decarboxylase.

"So I could draw off GABA, so you have more GABA. The GABA to glutamate ratio is shifted in favor of higher GABA. So there's a higher GABA to glutamate ratio when one is on the ketogenic diet... Glutamic acid decarboxylase is an enzyme that... But I think a key player in that is an elevation of GABA to glutamate. And we need glutamate to make GABA, right? But the enzyme is elevated and the pathways are shifted in favor of more glutamate to GABA, which has a stabilizing effect on your cell membrane and neuronal activity in general." (said at 0:38:40)

Preclinical studies demonstrate that a ketogenic diet elevates brain levels of gamma-aminobutyric acid (GABA) and increases the GABA-to-glutamate ratio, partially via the transcriptional upregulation of glutamic acid decarboxylase (GAD, such as GAD1/GAD67). Ketone body production, specifically beta-hydroxybutyric acid (BHB), has been shown in rodent models to inhibit histone deacetylases (HDAC1/HDAC2), upregulate GAD expression, and divert glutamate away from excitatory pathways and into GABA synthesis. Because direct mechanistic proof of GAD transcriptional upregulation and altered regional neurotransmitter ratios is derived from rodent models, the GRADE certainty of evidence is very low.

0:43:18Dominic D'Agostinosupportedmoderate

In a study of AC-1202 medium-chain triglyceride supplementation, elevated beta-hydroxybutyrate correlated with improved cognitive function in Alzheimer's patients without the APOE4 allele, but no improvement was observed in APOE4-positive patients.

"You're referring to the Henderson paper where they looked at AC-1202... So the finding was in that study, which is relatively small, that at least not with a diet, but using a ketone supplement that was formulated with 20 grams of medium-chain triglycerides, they gave it to their patients, I think, just once a day, and they did show fairly convincingly that the elevation of beta-hydroxybutyrate correlated with an improvement in cognitive function, but that correlation was not observed in the APOE4-positive group." (said at 0:43:18)

In a randomized, double-blind, placebo-controlled trial of 152 patients with mild to moderate Alzheimer's disease (Henderson et al., 2009), AC-1202 (a medium-chain triglyceride formulation) significantly elevated serum beta-hydroxybutyrate levels. Improvement in cognitive performance (ADAS-Cog score) and a significant correlation between elevated beta-hydroxybutyrate levels and cognitive improvement were observed specifically in patients who did not carry the APOE4 allele (E4(-)), whereas this therapeutic benefit was not seen in APOE4 carriers.

0:45:09Dominic D'Agostinosupportedmoderate

Ketone bodies increase cerebral blood flow by 30% to 40%.

"My student presented yesterday—I mean, she presented this week, but she graduated with her PhD yesterday, and her work showed that there's a remarkable increase in blood flow, and previous work has shown that ketone bodies can increase brain blood flow by 30 to 40%." (said at 0:45:09)

Published randomized clinical trials evaluating ketone body administration (specifically continuous intravenous infusion of 3-hydroxybutyrate / beta-hydroxybutyrate) have demonstrated that acute hyperketonemia increases global and regional cerebral blood flow by approximately 30% without altering cerebral oxygen consumption.

0:55:00Dominic D'Agostinosupportedvery low

In a rodent model of central nervous system oxygen toxicity, oral administration of a ketone ester delayed time to seizure toxicity by over 500%.

"And in that case, the rats were eating a high-carbohydrate standard rodent chow model, and we administered via, you know, an oral route uh a ketone supplement in the form of a ketone ester. That's probably one of the more powerful forms of exogenous ketones that that we've developed, and that had uh the ability to uh prevent CNS oxygen toxicity from happening for almost over 500% delay in that time to CNS oxygen toxicity." (said at 0:55:00)

In a 2013 preclinical study using adult male Sprague-Dawley rats exposed to hyperbaric oxygen (5 atmospheres absolute) to induce central nervous system oxygen toxicity, a single oral dose of the ketone ester 1,3-butanediol acetoacetate diester delayed latency to seizure by 574 ± 116% compared with water control. Because the evidence is derived entirely from animal models, certainty of evidence is graded as very low.

0:55:50Dominic D'Agostinosupportedvery low

Ketone supplementation in mice fed a high-carbohydrate diet reduced tumor burden and produced a 50% to 60% increase in survival in an aggressive metastatic glioblastoma model, effects exceeding calorie restriction controls.

"So we've also studied uh in our animal model of cancer, metastatic cancer, simply giving ketones to the animals on a high-carbohydrate diet, it was almost, you know, uh unexpected, the level of enhanced survival that we had uh with with ketone supplementation. This is a model of metastatic uh cancer, and the primary tumor was it was derived from a glioblastoma, a GBM... and it reduced tumor growth and proliferation... more sort of apoptosis in in the tumors that were there, but just overall there's just less tumor growth and less tumor burden and enhanced— most importantly, a 50 to 60% increase in survival time in animals that are supplemented with this... So we went back and we did a calorie restriction control experiment, and although there was a decrease in tumor, it was nothing like the ketone supplement." (said at 0:55:50)

The speaker accurately describes the findings of their 2014 preclinical study in mice implanted with VM-M3 cells (a model derived from murine glioblastoma that exhibits systemic metastatic spread). In that study, mice fed a standard high-carbohydrate diet supplemented with either 1,3-butanediol or a ketone ester demonstrated reduced tumor cell proliferation and viability, decreased tumor growth, and a 51% and 69% prolongation of survival, respectively, with anti-cancer effects occurring independently of calorie restriction or glucose lowering. Because the evidence is limited to an animal and in vitro model, the certainty of evidence for clinical application is very low.

0:59:06Rhonda Patrick (host)supportedmoderate

Lauric acid (C12) suppresses ghrelin in the gastrointestinal tract.

"HOST: You know what I just thought of? Um lauric acid, which is C12, um suppresses ghrelin in the gut, which is a hunger hormone." (said at 0:59:06)

Human clinical trials demonstrate that intraduodenal administration of lauric acid (dodecanoic acid, C12) suppresses circulating concentrations of ghrelin, an orexigenic (hunger-stimulating) gut peptide. In a randomized crossover study evaluating fatty acid chain lengths in healthy men, intraduodenal infusion of C12 markedly suppressed plasma ghrelin concentrations, whereas decanoic acid (C10) had no such effect. Subsequent trials examining intraduodenal nutrient infusions have further confirmed the ghrelin-suppressing effects of lauric acid in the gastrointestinal tract.

0:33:36Rhonda Patrick (host)supportedmoderate

Neuronal utilization of lactate spares glucose to be shunted into the pentose phosphate pathway, which generates NADPH needed for glutathione synthesis.

"neurons are actually using lactate, it's an energetically favorable source of energy, much like ketones. And so neurons like doing that because, one, it's easier, and two, because glucose can then be freed up to be shunted into the pentose phosphate pathway, which can be used to generate NADPH, which is important for glutathione, which makes sense." (said at 0:33:36)

The claim accurately describes the fundamental metabolic relationship between lactate uptake, glucose diversion to the pentose phosphate pathway (PPP), and NADPH generation for glutathione recycling in neurons. Neurons maintain low glycolytic rate because they continuously degrade the key glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3). When neurons utilize lactate supplied by astrocytes (via the astrocyte-neuron lactate shuttle) or external sources as a primary energetic fuel for oxidative phosphorylation, glucose is spared from glycolysis and directed into the PPP. The PPP metabolizes glucose to generate NADPH, which serves as an essential reducing equivalent for glutathione reductase to regenerate reduced glutathione (GSH) and combat oxidative stress.

0:44:26Dominic D'Agostinosupportedhigh

The medical food formulation Axona consists of caprylic triglyceride (C8).

"Axona, they use caprylic triglyceride, C8, which kind of makes a lot of ketones." (said at 0:44:26)

Axona (investigational name AC-1202) is a medical food formulation whose active ingredient is caprylic triglyceride (also known as tricaprilin or C8 medium-chain triglyceride). In the liver, caprylic triglyceride is metabolized into ketone bodies (such as beta-hydroxybutyrate and acetoacetate) to provide an alternative energy substrate for cerebral metabolism in cognitive impairment and Alzheimer's disease.

1:02:33Dominic D'Agostinosupportedhigh

Dichloroacetate (DCA) activates pyruvate dehydrogenase.

"And he's also looking at dichloroacetate, DCA, so it activates pyruvate dehydrogenase." (said at 1:02:33)

Dichloroacetate (DCA) is a well-characterized metabolic regulator that activates the pyruvate dehydrogenase (PDH) complex. It achieves this by acting as an inhibitor of pyruvate dehydrogenase kinase (PDK), an enzyme that normally phosphorylates and inactivates PDH. By blocking PDK-mediated phosphorylation, DCA keeps PDH in its unphosphorylated, active state, promoting the oxidation of pyruvate in the mitochondria and reducing lactic acid production.

1:06:00Rhonda Patrick (host)supportedvery low

Studies in mice show that administering antioxidants like vitamin E or N-acetylcysteine promotes accelerated tumor growth and metastasis in lung cancer and melanoma.

"And studies have shown, you know, that, you know, giving mice, you know, supplemental vitamin E, something that's going to, you know, potently sequester reactive oxygen species, actually allows tumors to grow faster. And this has been, you know, N-acetylcysteine, too, with metastatic melanoma, I think came out. Yeah, and then also there's one in lung cancer, I think it was the same publishing it." (said at 1:06:00)

Animal studies published in Science Translational Medicine demonstrated that dietary supplementation with antioxidants, including vitamin E and N-acetylcysteine (NAC), accelerated tumor progression in mouse models of B-RAF- and K-RAS-induced lung cancer (Sayin et al., 2014) and significantly increased lymph node metastasis in an endogenous mouse model of malignant melanoma (Le Gal et al., 2015). Because the underlying evidence is restricted to preclinical animal models, certainty is graded as very low.

1:11:17Rhonda Patrick (host)supportedmoderate

Mitochondria repair damaged components through mitochondrial fusion and fission by exchanging DNA and proteins.

"mitochondria have very elegant and beautiful way of repairing damage through fusion, right? Mitochondrial fusion and fission. This is a process I mean, this is how we are able to repair damaged mitochondria, because they're constantly fusing with healthy mitochondria, changing I mean, exchanging their DNA content, proteins, things like that, and fissioning back apart." (said at 1:11:17)

Mitochondrial fusion and fission operate as dynamic quality control mechanisms that enable functional complementation and mitochondrial maintenance. When mitochondria fuse, they exchange soluble matrix contents, proteins, and metabolites, and redistribute mitochondrial DNA (mtDNA) nucleoids across the network, buffering damaged components and restoring metabolic function. Asymmetric fission subsequently allows the segregation and selective degradation (via mitophagy) of severely damaged, non-repaired mitochondrial fragments.

1:14:48Dominic D'Agostinosupportedhigh

Gleevec (imatinib) is an effective targeted therapy for leukemia.

"whereas other types of, like for leukemia, for example, Gleevec works marvelously well, because it's targeting, you know, uh something that's very specific." (said at 1:14:48)

Imatinib (Gleevec) is a landmark targeted therapy that specifically inhibits the BCR-ABL tyrosine kinase, the oncogenic driver in chronic myeloid leukemia (CML). Long-term data from large phase 3 randomized trials (such as the IRIS study) demonstrate high rates of cytogenetic and molecular response and sustained overall survival (83.3% at 10 years and 89% at 5 years in newly diagnosed chronic-phase CML), transforming the prognosis of the disease.

1:26:46Rhonda Patrick (host)supportedhigh

Mature human red blood cells do not contain mitochondria.

"Your red blood cells have no mitochondria, and your red blood cells are important, right?" (said at 1:26:46)

The host's statement that human red blood cells (erythrocytes) do not contain mitochondria is fully supported by established cellular biology and clinical literature. During erythropoiesis (red blood cell maturation), reticulocytes clear their mitochondria via targeted autophagy (mitophagy) and eject their nuclei before entering peripheral circulation as mature erythrocytes. Consequently, mature human erythrocytes lack mitochondria (as well as nuclei and other internal organelles) and generate cellular ATP exclusively through anaerobic glycolysis.

1:19:50Dominic D'Agostinosupportedlow

Type 2 diabetics taking metformin have a 62% reduced risk of developing pancreatic cancer.

"The work the study's done with metformin and showing that people who type 2 diabetics that are taking metformin have a 62% less chance of getting pancreatic cancer." (said at 1:19:50)

The 62% risk reduction figure refers directly to a landmark hospital-based case-control study conducted at MD Anderson Cancer Center (Li et al., 2009), which found that diabetic patients who took metformin had a statistically significant 62% lower odds of developing pancreatic cancer compared to non-users (odds ratio 0.38, 95% CI 0.22–0.69). Broader systematic reviews and meta-analyses of observational cohorts and case-control studies confirm an inverse association between metformin use and pancreatic cancer risk, though pooled effect estimates generally range between 40% and 50% risk reduction. Because these findings are derived from observational epidemiological studies subject to residual confounding and indication biases rather than randomized controlled prevention trials, the GRADE certainty is low.

1:21:50Dominic D'Agostinosupportedhigh

Metformin can cause vitamin B12 deficiency.

"Uh and then another thing that creeps up could be uh vitamin B12 deficiency." (said at 1:21:50)

High-quality evidence from randomized controlled trials and systematic reviews confirms that long-term metformin therapy significantly reduces serum vitamin B12 concentrations and increases the risk of vitamin B12 deficiency. In a multicenter randomized placebo-controlled trial of patients with type 2 diabetes, metformin treatment resulted in an average 19% reduction in vitamin B12 levels and a 7.2 percentage point absolute increase in the risk of frank B12 deficiency over 4.3 years.

1:22:15Dominic D'Agostinosupportedmoderate

Metformin induces changes in the composition of the gut microbiome that contribute to its glucose-lowering effects in type 2 diabetes.

"It changes it changes the gut microbiome favorably. So Nature, there was a paper that came out about 2 weeks ago showing that there's a favorable shift in the gut microbiome with metformin, and that may explain its type 2 diabetic, you know, its glucose-lowering effects." (said at 1:22:15)

A double-blind randomized controlled trial published in Nature Medicine evaluated treatment-naive individuals with type 2 diabetes receiving metformin or placebo for four months. The study demonstrated that metformin significantly altered the gut microbiome composition. Furthermore, transferring fecal microbiota from metformin-treated human participants into germ-free mice directly improved glucose tolerance, establishing that metformin-induced shifts in the gut microbiota contribute causally to its antidiabetic and glucose-lowering effects.

1:22:45Dominic D'Agostinosupportedhigh

Metformin stimulates the activation of AMP-activated protein kinase (AMPK).

"Yeah, AMPK for sure, right? So without a doubt, I mean, it's it's it's mimicking many of the the pathways associated with calorie restriction and with fasting." (said at 1:22:45)

The scientific literature robustly supports that metformin stimulates the activation of AMP-activated protein kinase (AMPK). Activation of AMPK is one of the primary canonical mechanisms of action underlying metformin's downstream metabolic, cellular, and geroprotective effects, including the stimulation of fatty acid oxidation and inhibition of lipogenesis.

1:25:35Dominic D'Agostinosupportedlow

Metformin stimulates mitochondrial biogenesis.

"HOST: Does it biogenesis? GUEST1: It does, so yeah. So the the thought that, you know, it's kind of stimulating there's a hormetic effect, it's damaging the mitochondria, some people believe this, and uh and you get you get a secondary effect through that way" (said at 1:25:35)

The claim that metformin stimulates mitochondrial biogenesis is supported by published preclinical and mechanistic research. Studies show that metformin activates AMP-activated protein kinase (AMPK) and downstream signaling cascades (such as PGC-1α), promoting mitochondrial biogenesis and mitochondrial quality control in various cell models and tissues. However, evidence for this specific mechanism is primarily derived from cell culture and animal models rather than direct human clinical trials.

1:29:10Dominic D'Agostinosupportedmoderate

Ketones exert anti-catabolic and protein-sparing effects by inhibiting muscle proteolytic pathways.

"Uh and the ketones themselves are anti-catabolic or protein-sparing, so if you're in a state of ketosis, you're protecting glucogenic amino acids in skeletal muscle from being degraded, so you are uh, you know, as a metabolic fuel, but you're also there's evidence that you're inhibiting proteolytic enzymes and pathways that would otherwise be chewing up your muscle tissue over time." (said at 1:29:10)

Human experimental trials and physiological reviews support the claim that ketone bodies (specifically beta-hydroxybutyrate) have protein-sparing and anti-catabolic effects by attenuating skeletal muscle protein breakdown and amino acid oxidation. In a randomized crossover trial in humans undergoing inflammatory catabolic stress, beta-hydroxybutyrate infusion markedly suppressed muscle amino acid release and whole-body protein degradation.

1:20:56Dominic D'Agostinosupportedhigh

Metformin can cause lactic acidosis, particularly at higher doses or in patients with renal insufficiency or impaired liver function.

"Lactic acidosis could be a problem in higher doses for some people, maybe with renal insufficiency or impaired liver function." (said at 1:20:56)

Published literature and clinical pharmacology firmly establish that metformin can cause metformin-associated lactic acidosis (MALA), a rare but serious metabolic complication. Metformin is eliminated largely unchanged by the kidneys and reduces hepatic gluconeogenesis (which utilizes lactate). Consequently, higher doses, overdose, acute or chronic renal impairment (which leads to drug accumulation), and hepatic impairment (which impairs lactate clearance) are well-recognized risk factors and contraindications/cautions in clinical guidelines.

  • supports: Metformin-associated lactic acidosis: Bridging pharmacokinetic determinants, metabolic pat… (European journal of pharmacology 2026)
    "Although metformin possesses a favorable safety profile, a rare but serious adverse event known as metformin-associated lactic acidosis (MALA) may occur, particularly in patients with impaired renal clearance or predisposing comorbidities that favor drug retention... Crucially, MALA is fundamentally an accumulation disorder precipitated by an acute decline in kidney function rather than an intrinsic toxicity of metformin at therapeutic concentrations. Many precipitating factors, including acute kidney injury (AKI), chronic kidney disease (CKD), hepatic impairment, sepsis, hypoxia, and dehydration, substantially predispose individuals to this complication." (abstract, results, passage verified)
    pubmedfull study (doi)
1:22:00Dominic D'Agostinosupportedhigh

The human body's capacity to absorb vitamin B12 decreases with age.

"Our ability to absorb vitamin B12 as we age is decreased, so maybe a sublingual form or even B12 injections in people that are older." (said at 1:22:00)

The ability to absorb vitamin B12 (cobalamin), particularly food-bound cobalamin, decreases significantly with advancing age. Clinical absorption studies show significant reductions in protein-bound cobalamin absorption in older adults compared to younger adults, with further declines in individuals over 75 years of age. This age-related malabsorption is primarily driven by the increasing prevalence of atrophic gastritis, hypochlorhydria (reduced gastric acid secretion necessary to cleave cobalamin from dietary proteins), and frequent use of acid-suppressing medications.

1:28:16Dominic D'Agostinosupportedhigh

The primary substrates for gluconeogenesis include lactate, the glycerol backbone of triglycerides, and glucogenic amino acids from diet and skeletal muscle.

"so glycerol backbone of fatty acids or of triglycerides for sure, lactate yes, and amino acids, glucogenic amino acids in your diet uh also are a source of glucose, uh gluconeogenic amino acids in your skeletal muscle" (said at 1:28:16)

The primary substrates for gluconeogenesis in humans and other placental mammals are well established in biochemistry and metabolic physiology. As reviewed by Brosnan (2020, PMID 32652033), recognized gluconeogenic precursors capable of contributing net carbon to glucose synthesis include lactate and pyruvate, the glycerol backbone of triglycerides (lipids), and glucogenic amino acids (such as alanine and glutamine derived from dietary protein or released from skeletal muscle proteolysis during fasting or exercise). Extrahepatic studies in humans (e.g., Gerich et al. / Battezzati et al., PMID 12824085) also confirm that lactate, glycerol, and skeletal muscle-derived glucogenic amino acids (alanine and glutamine) serve as major endogenous substrates for hepatic and renal gluconeogenesis.

1:30:49Dominic D'Agostinosupportedmoderate

Ketone bodies are anti-catabolic, reducing the breakdown of skeletal muscle for glucogenic amino acids.

"ketones are anti-catabolic in that— HOST: Then you're probably not using the glucogenic amino acids as much from skeletal muscle. GUEST1: Yeah, not as much." (said at 1:30:49)

The claim that ketone bodies exert anti-catabolic effects by suppressing skeletal muscle breakdown and reducing the release of glucogenic amino acids is supported by human clinical trials and physiological studies. Administration of beta-hydroxybutyrate (3-hydroxybutyrate) significantly reduces muscle protein breakdown and systemic proteolysis under catabolic and fasting conditions. Furthermore, elevated ketone levels lower circulating levels and muscle release of primary glucogenic amino acids, such as alanine and glutamine, leading to reduced urinary nitrogen excretion and protein sparing.

1:33:30Rhonda Patrick (host)supportedmoderate

Research by Ralph DeBerardinis demonstrated using radiolabeling that cancer cells utilize glutamine predominantly for macromolecular synthesis such as fatty acids and proteins.

"some of the studies that were initially done by Ralph DeBerardinis when he was with Craig Thompson, later when he you established his own lab, um where he radio-labeled and showed that actually it was being used predominantly for macro- macromolecular synthesis and not for, you know, which is of course that makes sense because a lot of tumor cells aren't using their mito— GUEST1: Making fatty acids, proteins like for de novo synthesis." (said at 1:33:30)

Seminal in vitro work by Ralph DeBerardinis, Craig Thompson, and colleagues (2007) utilized 13C stable isotope labeling and NMR spectroscopy to show that transformed cancer cells consume glutamine at rates exceeding baseline protein and nucleotide synthesis requirements. Instead, glutamine is extensively metabolized via mitochondrial anaplerosis to sustain the tricarboxylic acid (TCA) cycle and provide NADPH to support macromolecular synthesis, including de novo fatty acid synthesis.

1:38:40Dominic D'Agostinosupportedmoderate

Glutamine supplementation is used in oncology to help patients recover from and combat the side effects of chemotherapy.

"glutamine has been used in in oncology, so— HOST: Yeah, glutamine for helping people with chemo, combating the issues with chemo. GUEST1: Yeah, glutamine has almost been like a staple, you know, so they give it to patients to help them recover." (said at 1:38:40)

Glutamine supplementation has been widely investigated and utilized in oncology supportive care to mitigate various adverse effects of chemotherapy, including chemotherapy-induced peripheral neuropathy (CIPN), oral mucositis, and gastrointestinal toxicity (such as diarrhea). While clinical trials and systematic reviews indicate potential benefits for these toxicities, systematic syntheses note that the certainty of evidence across indications remains low to moderate, warranting continued evaluation regarding standardized clinical recommendations.

1:39:00Rhonda Patrick (host)supportedmoderate

The gastrointestinal tract accounts for approximately 70% to 80% of the immune system.

"Your gut regulates the immune system as well. Your gut is like what, like 70-80% of your immune system, right? GUEST1: Yeah, it's huge" (said at 1:39:00)

The gastrointestinal tract houses the gut-associated lymphoid tissue (GALT), which constitutes the largest immunological organ in the human body. Published immunological reviews consistently establish that approximately 70% to 80% of the body's immune cells reside within the gut mucosal immune system.

1:44:05Dominic D'Agostinosupportedmoderate

Up to 40% to 50% of people experience gastrointestinal tolerability issues when consuming liquid MCT doses large enough to induce sustainable ketosis.

"Many people, you know, I would say, you know, up to 40 or 50% of people are going to have some tolerability issues with liquid MCTs, uh at least a big dose that gets you up into sustainable ketosis." (said at 1:44:05)

Clinical trials and systematic reviews evaluating medium-chain triglyceride (MCT) supplementation and MCT-based ketogenic therapies consistently demonstrate that gastrointestinal (GI) adverse effects—primarily diarrhea, abdominal cramping, bloating, and nausea—are common dose-limiting factors. Systematic analyses of ketogenic interventions indicate that approximately 40% to 43% of individuals experience GI side effects. Reviews on the ketogenic kinetics of MCTs confirm that large acute liquid doses necessary to achieve substantial ketosis (typically 15–20 g or higher in single boluses) frequently trigger GI distress, which is why clinical protocols recommend gradual dose titration.

7

No source found (not proven false)

0:18:56Rhonda Patrick (host)unverifiedvery low

Endotoxin release increases VLDL production because VLDL binds endotoxin, and endotoxin binds to ApoB and blocks LDL receptor recycling.

"Endotoxin released from the gut, one, it causes more VLDL production because VLDL soaks it up, so that's part of the reason why inflammation is also correlated with an increase in LDL, remember. It also binds to ApoB, it binds to where the LDL receptors bind so that LDL can't be recycled as well, so it kind of prevents—there's a lot of bad things about endotoxin being released." (said at 0:18:56)

No published record matching the claim that gut-derived endotoxin directly binds to ApoB at the LDL receptor binding site to block LDL receptor recycling, or that VLDL production increases because VLDL binds and soaks up endotoxin, was located; this does not prove the claim false.

0:40:20Dominic D'Agostinounverifiedvery low

Medium-chain fatty acids directly cross the blood-brain barrier and can be oxidized directly for fuel by the brain.

"Interestingly, we had a diet, too, that was high in medium-chain fatty acids, and although I heard medium-chain fatty acids could readily cross the blood-brain barrier—long-chain fatty acids typically don't, short-chain fatty acids sort of do—but we found very high levels of medium-chain fatty acids indicative of them, and these were normal, healthy animals. So when you take medium-chain fatty acids, they are readily—from the looks of our metabolomic data, just readily crossing the blood-brain barrier and capable of being used as fuel... So they're used—medium-chain fatty acids can be oxidized just for fuel, yeah, oxidative." (said at 0:40:20)

No published record matching the claim that medium-chain fatty acids directly cross the blood-brain barrier and can be oxidized directly for fuel by the brain was located; this does not prove the claim false.

0:45:41Dominic D'Agostinounverifiedvery low

Elevating ketone levels significantly elevates blood levels of adenosine, a potent vasodilator.

"We did laser Doppler blood flow measurement and showed that it spiked up considerably when we elevate ketones. One of the things—it was not dependent upon VEGF, so we looked at all the different factors. VEGF was not increased in the wound. And we looked at a couple other things that we thought would be increased. The one thing that stood out in the data was adenosine. So adenosine levels are significantly elevated... Regardless, adenosine is a very powerful vasodilator, and it's in significantly higher concentration in the blood, and that may be increasing the perfusion of tissues, peripheral tissues." (said at 0:45:41)

No published record matching the claim that elevating ketone levels significantly elevates blood levels of adenosine to promote vasodilation and tissue perfusion was located; this does not prove the claim false.

0:40:06Dominic D'Agostinounverifiedvery low

Ketone bodies readily cross the blood-brain barrier up to concentrations of approximately 5 to 7 millimolar before transport capacity becomes saturated.

"It's thought up to 5 millimolar, maybe 6, 7 millimolar, they can readily cross the blood-brain barrier. [0:40:12] HOST: You have to get that high before they start crossing? [0:40:14] GUEST1: No, like you start impeding once you get levels up that high." (said at 0:40:06)

No published record matching the claim that ketone body transport across the blood-brain barrier becomes saturated specifically at concentrations of approximately 5 to 7 millimolar was located; this does not prove the claim false.

1:09:00Dominic D'Agostinounverifiedvery low

Hereditary genetic factors account for approximately 7% to 10% of all cancers.

"the most we can link hereditary effect to to cancer is maybe about 10%, you know, 7% I think was the number that was is being thrown thrown around now, but about 10% of cancers are from a hereditary" (said at 1:09:00)

No published record matching the claim that hereditary genetic factors account for approximately 7% to 10% of all cancers was located; this does not prove the claim false.

1:09:47Dominic D'Agostinounverifiedvery low

Mitochondrial DNA has less robust DNA repair mechanisms and a higher density of coding regions compared to nuclear DNA.

"mitochondria have less uh of a robust DNA repair mechanism, and also the the DNA of the mitochondria have more coding regions." (said at 1:09:47)

No published record matching the claim that mitochondrial DNA has less robust DNA repair mechanisms and a higher density of coding regions compared to nuclear DNA was located; this does not prove the claim false.

1:44:20Dominic D'Agostinounverifiedvery low

MCT powder allows individuals to achieve blood ketone levels approximately twice as high as liquid MCT oil due to superior gastrointestinal tolerance and sustained release.

"the MCT powder uh I found was is you can get levels about twice as higher than you can with the oil, just simply because your GI tolerance is much better in a powder form. So it's formulated in a way that kind of allows a sustained, slower release of the MCT instead of uh a liquid" (said at 1:44:20)

No published record matching the claim that medium-chain triglyceride (MCT) powder produces blood ketone levels approximately twice as high as liquid MCT oil due to improved gastrointestinal tolerance and sustained release was located; this does not prove the claim false.

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.