DavidPerlmutterMD · 2025-04-21 · David Perlmutter (host), Steven Gundry
The Gut-Brain Paradox: Secrets To Restoring Health | Steven Gundry
35 research-tied claims examined: 8 contradicted 4 overstated 4 context 15 supported 4 unverified
4 Overstated
Glyphosate selectively kills gut bacteria responsible for the tryptophan pathway.
"And then to come to find out that these tryptophan pathway bacteria are selectively killed by glyphosate, the active ingredient in Roundup." (said at 0:26:40)
Glyphosate inhibits 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), an enzyme in the shikimate pathway used by plants and some microorganisms to synthesize aromatic amino acids, including tryptophan. However, stating that bacteria responsible for this pathway are 'selectively killed' in the gut overstates the evidence. Metagenomic and metatranscriptomic analyses of the human gut microbiome demonstrate that most gut bacterial species lack a complete shikimate pathway, rely on dietary aromatic amino acids (auxotrophy), or carry glyphosate-insensitive (class II) EPSPS enzymes, making them largely unaffected. Furthermore, while in vivo rodent studies confirm that glyphosate can inhibit the EPSPS enzyme in the gut (evidenced by the accumulation of shikimic acid in the caecum), this enzymatic inhibition does not cause a selective kill-off or major depletion of the microbial community.
Fecal microbiota transplants from depressed human donors into healthy rats induce depressive behavior in the rats, and transplants from healthy humans into depressed rats reverse their depression.
"And we know from animal experiments that we can take a happy rat and have it eat poop from a depressed individual and the rat will become depressed. Uh we joke rats love to eat poop. So and and conversely we can take a happy people's microbiome and have a depressed rat eat that and they'll become happy." (said at 0:27:40)
Preclinical animal research demonstrates that fecal microbiota transplantation (FMT) from humans diagnosed with major depressive disorder into microbiota-depleted rodents induces depressive-like and anxiety-like behaviors (such as anhedonia) as well as altered tryptophan metabolism (PMID: 27491067). However, the claim oversimplifies and overstates the literature in several ways: the experiments involve oral gavage into antibiotic-depleted or germ-free rodent models rather than animals freely eating feces to transfer phenotypes, and while healthy human microbiota transfers have been used as non-depressed control baselines, evidence showing complete reversal or 'curing' of pre-existing depression in rodents by transplanting healthy human microbiota is considerably more preliminary and conditional. Evidence is restricted to rodent models, yielding very low certainty for human clinical relevance.
Human studies in alcohol rehabilitation show that individuals with the most dysbiotic gut microbiome have the highest rates of treatment failure, whereas those with the least dysbiotic microbiome have the best outcomes.
"there's actually beautiful work in human studies with alcohol uh rehab. People who have the most dysbiotic alcohol seeking microbiome are the biggest failures in treatment and the people who have the least alcohol seeking microbiome are the best chances to make it through." (said at 0:30:32)
Clinical studies (notably seminal work by Leclercq et al., 2014) have demonstrated an association between gut microbiota dysbiosis, increased intestinal permeability, and higher psychological markers of relapse risk (such as elevated alcohol craving, depression, and anxiety) in alcohol-dependent patients undergoing short-term rehabilitation/detoxification. However, characterizing this as definitive proof that an 'alcohol-seeking microbiome' dictates treatment failure versus success overstates the findings. The available human research primarily evaluates surrogate psychological markers (craving and negative affect during early abstinence) in small observational cohorts rather than long-term clinical treatment failure or relapse endpoints, and the label 'alcohol seeking microbiome' is an oversimplification of complex dysbiotic shifts.
- partial: Intestinal permeability, gut-bacterial dysbiosis, and behavioral markers of alcohol-depend… (Proceedings of the National Academy of Sciences of the United States of America 2014) · cited 978x in the literature
"We found that some, but not all, alcohol-dependent subjects developed gut leakiness, which was associated with higher scores of depression, anxiety, and alcohol craving after 3 wk of abstinence, which may be important psychological factors of relapse. Moreover, subjects with increased gut permeability also had altered composition and activity of the gut microbiota." (abstract, results, passage verified)
pubmedfull study (doi)
Most motorcycle accident victims are infected with Toxoplasma gondii.
"And what's really wild is that most most motorcycle accident victims are infected with toxoplasmosis." (said at 0:37:05)
While observational studies and meta-analyses have found a statistically significant association between latent Toxoplasma gondii infection and an increased risk of traffic accidents (with pooled odds ratios around 1.69 and a population attributable fraction around 17%), it is not true that "most" motorcycle or traffic accident victims are infected. Studies specifically evaluating motorcycle crash victims report seroprevalence rates far below a majority (e.g., 12.5% in a case-control study).
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.