8 Needs context
The diagnostic standards for normal bone density were changed, categorizing millions of people as having osteopenia or osteoporosis.
"But also realize not too long ago they changed the normals for osteoporosis and instantly put millions of people in the state of having osteopenia or osteoporosis just by changing what normal is." (said at 0:11:27)
The statement refers to the 1994 World Health Organization (WHO) establishment of densitometric diagnostic criteria for osteoporosis and osteopenia. The WHO defined 'normal' bone mineral density (BMD) using young adult peak bone mass as the reference point (T-score >= -1.0), with osteopenia defined as a T-score between -1.0 and -2.5, and osteoporosis defined as a T-score of -2.5 or lower. Because BMD naturally declines with age, comparing postmenopausal individuals against healthy young adults classified millions of older adults as having low bone mass or osteoporosis. However, this established the standardized international definitions rather than altering an existing standard to arbitrarily reclassify individuals.
TUDCA is an antibacterial bile salt.
"The other thing I would take is I would take TUDCA on an empty stomach twice a day. That bile salt is antibacterial." (said at 0:13:12)
Bile acids and bile salts as a chemical class possess antimicrobial and antibacterial properties that help regulate the gut microbiome, with direct in vitro activity demonstrated for compounds such as ursodeoxycholic acid (UDCA), deoxycholic acid (DCA), and chenodeoxycholic acid (CDCA). However, tauroursodeoxycholic acid (TUDCA) is the hydrophilic taurine-conjugated form of UDCA; conjugated and hydrophilic bile acids generally exhibit weaker direct antibacterial action than unconjugated, more hydrophobic bile acids. While bile acids broadly influence microbial composition and possess antibacterial properties in preclinical models, there is no evidence establishing oral TUDCA supplementation as a clinically effective antibacterial agent in humans.
- partial: Antibacterial action of bile acids against Helicobacter pylori and changes in its ultrastr… (Journal of gastroenterology 1999) · cited 47x in the literature
"We found that only the unconjugated form of dihydroxy bile acid has antibacterial activity. The minimum inhibitory concentration of deoxycholic acid is 200-400 microg/ml, that of chenodeoxycholic acid is similar to that of deoxycholic acid, and that of ursodeoxycholic acid is 400-800 microg/ml." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Bile Acids: Major Regulator of the Gut Microbiome. (Microorganisms 2022) · cited 51x in the literature
"The different degrees of hydrophobicity and acidity of individual bile acids may affect their antimicrobial properties. We examined the antimicrobial effects of different bile acids on various microorganisms in vitro and confirmed whether these remain consistent in vivo. Using human bile acids, including ursodeoxycholic acid, cholic acid, chenodeoxycholic acid, deoxycholic acid, and lithocholic acid, a disc diffusion test was performed, and a rodent model was created to determine the antimicrobial effects of each bile acid. Each bile acid showed different microbial inhibitory properties." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Antiviral and virucidal activities against SARS-CoV-2 and antibacterial properties of bile… (RSC advances 2025) · cited 1x in the literature
"Bile acids DCA (5), UDCA (9), and CDCA (13) exhibited antibacterial activity against Gram-positive bacteria ( Bacillus cereus , Staphylococcus aureus , Staphylococcus epidermidis , and Enterococcus faecalis ) and against a Gram-negative bacterium ( Escherichia coli )." (abstract, results, passage verified)
pubmedfull study (doi)
TUDCA is mostly water-soluble rather than fat-soluble, preventing it from aiding fat digestion.
"TUDCA is very, very different than regular bile salts. It's mostly water soluble. It's not fat soluble, which means it's not something that's going to help you digest fats at all." (said at 0:20:34)
The claim is partially accurate regarding the physical chemical properties of tauroursodeoxycholic acid (TUDCA), but inaccurate regarding its functional ability to aid in fat digestion. TUDCA (and its parent bile acid ursodeoxycholic acid, UDCA) is indeed a highly hydrophilic (water-soluble) bile acid compared to typical endogenous bile salts such as taurocholate or taurochenodeoxycholate. Because of its hydrophilic nature, TUDCA forms larger, less efficient mixed micelles for solubilizing hydrophobic lipids such as cholesterol, leading to lower rates of intestinal uptake compared to more hydrophobic bile salts (PMID: 7093350). However, stating that TUDCA "is not going to help you digest fats at all" is incorrect. Clinical research shows that supplementation with ursodeoxycholic acid species improves lipid digestion and absorption in patients with lipid malabsorption (such as cystic fibrosis patients with mild liver involvement) (PMID: 26882172), though high-dose UDCA supplementation in healthy individuals can modestly alter or decrease the efficiency of triglyceride absorption relative to standard hydrophobic bile salt pools (PMID: 6719039). Therefore, while TUDCA is predominantly hydrophilic and less efficient than hydrophobic bile salts at micelle formation, it still participates in fat solubilization and digestion.
Blood pH is slightly alkaline, the stomach is highly acidic, the large intestine is acidic, and the small intestine is alkaline.
"You have the blood is slightly alkaline, very slightly. You have the stomach, super acid, large intestine, acid, small intestine, alkaline." (said at 0:30:49)
The host's broad characterization of physiological pH across body compartments is generally accurate in describing relative pH differences, but oversimplifies the internal gradients of the intestinal tract. Normal blood pH is tightly regulated and slightly alkaline (7.35–7.45). The stomach is highly acidic (fasting luminal pH approximately 1.0–2.5). In the small intestine, intraluminal pH is slightly acidic to neutral in the duodenum and proximal jejunum (pH ~6.0–6.6) and gradually increases to slightly alkaline in the terminal ileum (~7.4–7.5). Upon entry into the large intestine (cecum and proximal colon), pH drops back to acidic levels (~5.7–6.4) due to bacterial fermentation of carbohydrates into short-chain fatty acids, before rising toward near-neutral (6.7–7.0) in the distal colon and rectum. Thus, while the large intestine's proximal segment is acidic compared to the terminal ileum and the terminal small intestine is alkaline, both the small and large intestines span a continuum from acidic/neutral to neutral/alkaline.
Ox bile is alkaline and can neutralize stomach acid.
"Yes, it is true that um ox bile is alkaline. So that can neutralize the stomach acid." (said at 0:32:21)
Fresh mammalian bile (including bovine/ox bile) and biliary secretions are slightly alkaline to neutral (typically pH 7.4–8.5 due to bicarbonate content), and along with pancreatic and duodenal secretions, biliary bicarbonate contributes to buffering acidic chyme entering the duodenum. However, ox bile supplements primarily consist of dried bile salts/acids, which have minimal acid-buffering capacity compared to standard antacids. Furthermore, in the digestive tract, duodenal neutralization is primarily driven by pancreatic and duodenal mucosal bicarbonate rather than bile alone, and the ingestion of bile salts into an acidic stomach can cause mucosal irritation rather than acting as a therapeutic acid neutralizer.
Having sufficient stomach acid stimulates the liver to produce more bile.
"if you have enough stomach acid that will actually tell your liver to make more bile." (said at 0:32:21)
When acidic chyme from the stomach enters the duodenum, duodenal acidification triggers the release of the hormone secretin into the bloodstream. Secretin acts on the liver's biliary ductular epithelial cells (cholangiocytes) to stimulate the secretion of bicarbonate and water, significantly increasing total hepatic bile flow (ductular choleresis) to help neutralize acid in the small intestine. However, stomach acid and secretin stimulate the secretion of water and bicarbonate into the bile ducts (increasing bile volume and output), rather than stimulating hepatocytes to synthesize more bile acids (which is regulated primarily by bile acid return via the enterohepatic circulation and FXR signaling).
Arugula is the food with the highest concentration of dietary nitrate/nitric oxide precursors, followed by cacao and beetroot juice powder.
"The food that has the most nitric oxide would be arugula. Uh and then you can also do cacao and then um um beet beetroot uh juice powder also has it." (said at 0:42:35)
Arugula (rocket) and leafy green vegetables contain the highest concentrations of inorganic nitrate, followed by root vegetables like beetroot, which act as dietary precursors for endogenous nitric oxide synthesis via the enterosalivary nitrate-nitrite-nitric oxide pathway. Foods do not contain meaningful amounts of nitric oxide gas directly. Furthermore, cacao does not contain high concentrations of inorganic nitrate precursors; its modulation of nitric oxide bioavailability occurs through cocoa flavanol activation of endothelial nitric oxide synthase rather than providing direct nitrate content.
- context: Development of a reference database for assessing dietary nitrate in vegetables. (Molecular nutrition & food research 2017) · cited 101x in the literature
"Nitrate from vegetables improves vascular health with short-term intake." (abstract, background, passage verified)
pubmedfull study (doi) - context: A food composition database for assessing nitrate intake from plant-based foods. (Food chemistry 2022) · cited 50x in the literature
"Despite substantial variations, leaf vegetables were the top nitrate-containing foods, followed by stem & shoot vegetables, herbs and spices, root vegetables, flower vegetables, tuber vegetables, nuts, fruit vegetables, legume/seed vegetables, fruits and cereals." (abstract, results, passage verified)
pubmedfull study (doi)
Entering ketosis causes a temporary spike in uric acid, which is an antioxidant with greater antioxidant capacity in human blood than vitamin C.
"There is going to be a temporary spike in uric acid. Uric acid is not all bad. It's a very powerful antioxidant, even more powerful than vitamin C in your blood." (said at 0:55:34)
Entering ketosis often causes a transient increase in circulating serum uric acid due to competitive inhibition between ketone bodies (such as acetoacetate and beta-hydroxybutyrate) and uric acid for renal tubular secretion transporters (such as OAT4 and URAT1); randomized trials and meta-analyses show that this elevation is typically temporary and does not persist as a long-term increase. Furthermore, uric acid functions as a major endogenous antioxidant in human plasma, contributing significantly to total aqueous antioxidant capacity due to its relatively high physiological concentrations. However, calling it 'more powerful than vitamin C' requires biochemical qualification: in vitro and plasma studies demonstrate that ascorbic acid (vitamin C) is the primary and most effective aqueous-phase antioxidant per molecule protecting plasma lipids against peroxidative damage, reacting before urate is consumed.
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.