Dr. Eric Berg DC · 2026-07-17 · Eric Berg (host), Steve, Tahira, Manuel, Piba, Canal

The Dr. Berg Show LIVE - July 17, 2026

38 research-tied claims examined: 3 contradicted 1 contradicted online 4 overstated 7 context 19 supported 4 unverified

Contradicted by research

0:15:07 Eric Berg (host)contradictedmoderate

A deficiency of concentrated bile salts entering the small intestine promotes constipation, as bile salts assist digestion and prevent constipation.

"Bile salts actually help they're kind of they help you digest. They help uh prevent constipation. So I think what happened is they remove the gallbladder. Now you just have this trickling effect of bile that's going in the small intestine. You have no concentrated amount anymore that can squeeze out when you eat. So, you're going to be deficient and then that leads to constipation." (said at 0:15:07)

While the host is correct that bile salts act as natural osmotic and stimulant laxatives that facilitate digestion and stimulate colonic motility, the claim that cholecystectomy causes a bile salt deficiency that leads to constipation is contradicted by medical evidence. Following gallbladder removal (cholecystectomy), bile trickles continuously into the small intestine rather than being stored and concentrated. This continuous flow increases bile acid exposure in the colon, which is known to cause increased stool frequency or post-cholecystectomy diarrhea in sensitive individuals, rather than constipation due to bile deficiency.

contradicts: Effect of cholecystectomy on bowel function: a prospective, controlled study. (Gut 1999) · cited 53x in the literature
"In cholecystectomised women, stated bowel frequency increased, on average by one movement a week, and fewer subjects felt that they became constipated." (abstract, results, passage verified)
pubmed full study (doi)
contradicts: [Gastrointestinal function following cholecystectomy]. (Ugeskrift for laeger 2005) · cited 1x in the literature
"Bile acid malabsorption is increased postoperatively, probably giving rise to diarrhea in a few sensitive individuals." (abstract, passage verified)
pubmed
supports: The receptor TGR5 mediates the prokinetic actions of intestinal bile acids and is required… (Gastroenterology 2013) · cited 353x in the literature
"The receptor TGR5 mediates the effects of BAs on colonic motility, and deficiency of TGR5 causes constipation in mice. These findings might mediate the long-known laxative properties of BAs, and TGR5 might be a therapeutic target for digestive diseases." (abstract, conclusions, passage verified)
pubmed full study (doi)
supports: Elobixibat and its potential role in chronic idiopathic constipation. (Therapeutic advances in gastroenterology 2014) · cited 92x in the literature
"Bile acids (BAs) and the enterohepatic BA circulation modulate colonic secretion and motility that affect transit. BAs in the colon have a dual action as osmotic and stimulant agents." (abstract, passage verified)
pubmed full study (doi)

0:42:48 Eric Berg (host)contradictedvery low

Yeast overgrowth produces an alkaline byproduct of ammonia as a survival mechanism.

"The other thing that's in my mind with ammonia is a yeast overgrowth, but that would only occur if you're consuming a lot of sugar and starch, which I don't think you are. But having that yeast overgrowth just gives off a byproduct of ammonia, which is very alkaline. That's a survival mechanism." (said at 0:42:48)

Preclinical in vitro and cellular studies confirm that pathogenic yeast such as Candida albicans can extrude ammonia as an alkaline byproduct to neutralize acidic environments (such as macrophage phagolysosomes), promoting hyphal morphogenesis and fungal survival. However, the speaker's assertion regarding the metabolic driver is inverted: research demonstrates that ammonia release and extracellular alkalinization are specifically induced by carbon/glucose deprivation—forcing the yeast to catabolize amino acids as an alternative carbon source—rather than by high sugar or starch consumption.

supports: The fungal pathogen Candida albicans autoinduces hyphal morphogenesis by raising extracell… (mBio 2011) · cited 372x in the literature
"Alkalinization is linked to carbon deprivation, as it occurs in glucose-poor media and requires exogenous amino acids... We propose that nutrient-deprived C. albicans cells catabolize amino acids as a carbon source, excreting the amino nitrogen as ammonia to raise environmental pH and stimulate morphogenesis, thus directly contributing to pathogenesis." (abstract, results)
pubmed full study (doi)
supports: The Candida albicans ATO Gene Family Promotes Neutralization of the Macrophage Phagolysoso… (Infection and immunity 2015) · cited 59x in the literature
"We have shown that amino acid catabolism allows the cell to neutralize the phagolysosome and initiate hyphal growth. We show here that members of the 10-gene ATO family, which are induced by phagocytosis or the presence of amino acids in an Stp2-dependent manner and encode putative acetate or ammonia transporters, are important effectors of this pH change in vitro and in macrophages." (abstract, results, passage verified)
pubmed full study (doi)

1:01:07 Eric Berg (host)contradictedmoderate

During menopause, a decline in sex hormones impairs protein synthesis and shifts the body into a catabolic state.

"What happens during menopause is you have the sex hormones start going way, way down. And yes, those can affect hair, protein, especially the synthesis of protein. Um, your body now is in more of a state of breakdown mode. It's called a catabolic mode." (said at 1:01:07)

The claim that the decline in sex hormones during menopause impairs basal protein synthesis is contradicted by clinical evidence. Direct measurements of human muscle protein turnover demonstrate that basal muscle protein fractional synthesis rates (FSR) are not reduced in postmenopausal women compared to premenopausal women; rather, basal synthesis is typically equivalent or up to 20% faster. Furthermore, clinical trials show that estradiol replacement does not stimulate muscle protein synthesis in postmenopausal women, whereas progesterone and testosterone do. While menopause is associated with a gradual loss of lean mass and potential blunting of the anabolic response to protein intake or resistance exercise, as well as possible increases in protein breakdown markers, the underlying physiological mechanism is not an impairment of baseline protein synthesis.

contradicts: Testosterone and progesterone, but not estradiol, stimulate muscle protein synthesis in po… (The Journal of clinical endocrinology and metabolism 2014) · cited 126x in the literature
"The muscle protein fractional synthesis rate was approximately 20% faster, and MYOD1, FST, and FOXO3 mRNA expressions were approximately 40%-90% greater (all P<.05) in postmenopausal than premenopausal women. In postmenopausal women, both T and progesterone treatment increased the muscle protein fractional synthesis rate by approximately 50% (both P<.01), whereas it was not affected by estradiol treatment and was unchanged in the control group." (abstract, results, passage verified)
pubmed full study (doi)
context: Menopause, Female Sex Hormones, Skeletal Muscle Mass and Muscle Protein Turnover in Humans… (Journal of cachexia, sarcopenia and muscle 2026) · cited 7x in the literature
"Assessment on changes to muscle protein turnover is largely limited to short-term measures of muscle protein synthesis (MPS), which may be elevated in older women versus younger women (n = 3/7) or age-matched males (n = 4/5). MPS responses to anabolic stimuli, such as resistance exercise (n = 3/4) or protein ingestion (n = 3/6), may be blunted in older women." (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.