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

Overstated

0:31:42 Dominic 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.

partial: Ketogenic diet slows down mitochondrial myopathy progression in mice. (Human molecular genetics 2010) · cited 192x in the literature
"The diet did not, however, significantly affect the mtDNA quality or quantity, but rather induced mitochondrial biogenesis and restored liver lipid levels." (abstract, results, passage verified)
pubmed full study (doi)
partial: Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mic… (FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2012) · cited 130x in the literature
"Feeding the KE diet for up to 1 mo increased the number of mitochondria and doubled the electron transport chain proteins, uncoupling protein 1, and mitochondrial biogenesis-regulating proteins in the interscapular brown adipose tissue (IBAT)." (abstract, results, passage verified)
pubmed full study (doi)

0:48:47 Dominic 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.

partial: TSPO PET upregulation predicts epileptic phenotype at disease onset independently from chr… (NeuroImage. Clinical 2021) · cited 24x in the literature
"By applying multivariate analysis, TSPO PET imaging at disease onset identified three KASE groups with significantly different spontaneous recurrent seizures (SRS) burden (defined as rare SRS, sporadic SRS, and frequent SRS) (p = 0.003)." (abstract, results, passage verified)
pubmed full study (doi)
context: Identification of neuro-inflammatory biomarkers through non-invasive advanced neuroimaging… (Epilepsy & behavior : E&B 2025) · cited 2x in the literature
"These biomarkers could be used as diagnostic, predictive, and therapeutic targets. Moreover, they can be used to delineate epileptic foci in the presurgical evaluation of refractory epileptic patients. However, these studies are still in the preclinical phase, requiring further research in this field." (abstract, conclusions, passage verified)
pubmed full study (doi)

1:34:10 Rhonda 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.

partial: Oxidation of glutamine by the splanchnic bed in humans. (American journal of physiology. Endocrinology and metabolism 2000) · cited 69x in the literature
"we determined that 27 +/- 2% of the enterally delivered phenylalanine and 64 +/- 2% of the glutamine were removed on the first pass by the splanchnic bed." (abstract, results, passage verified)
pubmed full study (doi)
partial: Free and protein-bound glutamine have identical splanchnic extraction in healthy human vol… (American journal of physiology. Gastrointestinal and liver physiology 2001) · cited 33x in the literature
"Splanchnic extraction of glutamine reached 62.5 +/- 5.0% and 66.7 +/- 3.9% after administration of (15)N-labeled oat proteins and the mixture of free amino acids, respectively." (abstract, results, passage verified)
pubmed full study (doi)
partial: Response of glutamine metabolism to exogenous glutamine in humans. (The American journal of physiology 1995) · cited 97x in the literature
"Splanchnic glutamine extraction (determined from [13C]glutamine appearance into systemic blood) reached 74 +/- 4 and 53 +/- 5% during the enteral infusion of tracer alone and in combination with a large load of glutamine, respectively. Glutamine infusion was associated with increased plasma glutamine concentration (from 630 +/- 50 to 1,297 +/- 75 microM)" (abstract, results, passage verified)
pubmed full study (doi)

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.