HoldsUp

Dr. Eric Berg DC · 2026-07-31 · Eric Berg (host), Steve (host), Karen, Diana, Tonya

The Dr. Berg Show LIVE - July 31, 2026

41 research-tied claims examined: 3 contradicted 6 overstated 4 context 20 supported 8 unverified

20

Supported by research

0:08:29Eric Berg (host)supportedmoderate

Bile released upon eating has antimicrobial properties that clear out bacteria in the small intestine, protecting against SIBO.

"normally what happens is when you have a bile release when you eat, that bile is very antimicrobial. It uh is one of the purposes not not just to break down fat, but to clear out the bacteria in the small intestine." (said at 0:08:29)

Bile and bile acids possess well-documented direct and indirect antimicrobial properties that regulate the small intestinal microbiota and inhibit excessive bacterial proliferation. Physiological bile secretion helps maintain low bacterial counts in the upper small bowel, and deficiencies in bile acid flow or synthesis are recognized risk factors for small intestinal bacterial overgrowth (SIBO). Furthermore, preliminary randomized clinical trial data demonstrate that bile acid therapy (such as ursodeoxycholic acid) can significantly reduce breath test markers of bacterial overgrowth and alleviate associated digestive symptoms.

0:08:52Eric Berg (host)supportedhigh

Approximately 90 percent of bile is reabsorbed at the end of the small intestine and recycled.

"right before it goes in the large, it gets reabsorbed and recycled. So, 90% of your bile is recycled because we need it." (said at 0:08:52)

Physiological evidence confirms that bile acids undergo extensive enterohepatic circulation, where approximately 90% to 95% of bile acids are reabsorbed in the terminal ileum (the end of the small intestine) and returned via the portal vein to the liver for recycling, with only about 5% excreted in the feces.

0:09:27Eric Berg (host)supportedhigh

Approximately 80 percent of heart attacks are caused by a blood clot rather than plaquing alone.

"About 80% of heart attacks uh come from um a clot versus like plaquing." (said at 0:09:27)

The speaker's statement is accurate. Landmark clinical and arteriographic studies established that approximately 80% of acute transmural myocardial infarctions evaluated within the first 6 hours of symptom onset are precipitated by acute thrombus (blood clot) formation superimposed on an underlying atherosclerotic lesion, rather than by fixed plaque narrowing alone.

0:09:45Eric Berg (host)supportedmoderate

Elevated blood sugar damages the single-cell endothelial lining of blood vessels within a short period, leading to inflammation and clotting.

"when your blood sugars go up and it goes to your uh vessels uh it kind of just within a very short period of time, it just damages that very delicate single-cell endothelial wall of that's supposed to protect you. And then you get all sorts of uh potential problems and inflammation and which leads to clotting and heart attacks." (said at 0:09:45)

Acute elevations in blood glucose rapidly induce endothelial dysfunction, oxidative stress, inflammation, and a prothrombotic state. Experimental human studies, such as glucose clamp protocols and oral glucose challenges, demonstrate that acute hyperglycemia impairs endothelium-dependent flow-mediated vasodilation within hours and significantly increases circulating adhesion molecules (VCAM-1, ICAM-1, E-selectin), inflammatory cytokines (such as IL-6), and prothrombotic markers (such as plasminogen activator inhibitor-1, PAI-1).

0:11:32Eric Berg (host)supportedmoderate

Iron from spinach is poorly absorbed by the body compared to heme-based iron from meat.

"And if you think you're getting your iron from spinach because Popeye the Sailor Man was did that as well, then uh you're not getting the right kind because you're going to be getting something that doesn't really absorb that well." (said at 0:11:32)

Dietary iron exists primarily in two forms: heme iron, derived from hemoglobin and myoglobin in meat, and non-heme iron, found in plant sources such as spinach. Non-heme iron has substantially lower bioavailability and absorption efficiency in humans (typically 2% to 15%) compared to heme iron (typically 15% to 35%). In human randomized crossover isotope trials, non-heme iron absorption from spinach meals is relatively low and inhibited by the presence of polyphenols and calcium.

0:12:02Eric Berg (host)supportedhigh

The human body has no active physiological mechanism for excreting excess iron.

"There's a lot of people that we have no mechanism of getting rid of excess iron. So, it's it's a big problem." (said at 0:12:02)

The host's statement that the human body has no active physiological mechanism for excreting excess iron is accurate and reflects a fundamental principle of human iron homeostasis. Because humans lack a regulated pathway to actively excrete excess iron, systemic iron balance is regulated almost entirely at the level of intestinal absorption and cellular storage through pathways controlled by hormones such as hepcidin. Uncontrolled iron absorption or excessive iron administration can therefore lead to tissue overload.

0:12:25Eric Berg (host)supportedmoderate

Excess iron accumulation can cause liver inflammation and cirrhosis.

"iron is a is a big big problem for people um especially men. It can create um inflammation um of the liver, cirrhosis, things like that." (said at 0:12:25)

Hepatic iron overload, as seen in primary conditions like hereditary hemochromatosis as well as secondary iron overload disorders, is established to cause liver injury, inflammation, progressive fibrosis, and cirrhosis. Men are clinically at higher risk of symptomatic iron accumulation and end-organ damage earlier in life because they lack the physiological blood loss associated with menstruation and pregnancy. Excess iron promotes oxidative stress, lipid peroxidation, and hepatocyte necrosis, which trigger inflammatory responses and hepatic stellate cell activation leading to fibrosis and cirrhosis.

0:13:30Eric Berg (host)supportedmoderate

Zinc is a required cofactor for vitamin A function in the body.

"it could be that you don't have enough of the cofactor for vitamin A, which is zinc." (said at 0:13:30)

Zinc is an established essential cofactor and regulatory nutrient for multiple steps in vitamin A metabolism and function. Specifically, zinc is a cofactor for retinol dehydrogenase (retinene reductase), the zinc-metalloenzyme that converts retinol to retinal in the visual cycle, and is required for the hepatic synthesis and secretion of retinol-binding protein (RBP), which transports vitamin A throughout the circulation. Zinc deficiency can consequently impair vitamin A mobilization and functional utilization (such as dark adaptation/night vision) even when dietary vitamin A intake is sufficient.

  • supports: The vitamin A-zinc connection: a review. (Annals of the New York Academy of Sciences 1980) · cited 106x in the literature
    "In regard to retinol-binding protein, it appears from the animal studies that zinc deficiency per se has an effect on both the plasma and liver RBP concentrations. We have hypothesized that zinc deficiency impairs RBP synthesis. It is speculated that only severe zinc deficiency results in a deficit of a sufficient magnitude for impairment of vitamin A metabolism at the cellular level. For example, retinene reductase, an apparent zinc-metallo alcohol dehydrogenase of the retina, appears to be sensitive to a severe zinc deficiency in animal studies. In humans, impaired dark adaptation may be a result of inadequate supplies of the metabolizable zinc necessary to maintain the activity of the enzyme system. Thus, the conversion (dehydrogenation) of vitamin A alcohol to vitamin A aldehyde is impaired, with a resulting abnormality in dark adaptation, i.e., night blindness." (abstract, results, passage verified)
    pubmedfull study (doi)
0:14:23Eric Berg (host)supportedmoderate

Resistance training increases muscle uptake of leucine for up to 24 hours to stimulate muscle protein synthesis.

"if you increase uh more resistance training, like weight training, and work up to that, it apparently opens up the muscles for like 24 hours to be able to take in more um leucine, which is amino acid in meat, uh animal meat." (said at 0:14:23)

Human metabolic and exercise physiology studies confirm that resistance exercise enhances the muscle's sensitivity to amino acids (particularly leucine) and increases the expression of amino acid transporters (such as LAT1/SLC7A5) for up to 24 hours post-exercise. This heightened sensitivity and transporter upregulation allow muscle to more effectively utilize circulating leucine and stimulate myofibrillar protein synthesis following protein ingestion over a prolonged 24-hour recovery window.

0:22:12Eric Berg (host)supportedmoderate

Selenium supports the enzymatic conversion of T4 to T3 and lowers thyroid peroxidase (TPO) autoantibody levels in Hashimoto's thyroiditis.

"selenium helps not just the conversion from T4 to T3... And secondly, most thyroid is um autoimmune, Hashimoto's. And so if you have autoantibodies to it's called something called TPO, which is um part of the thyroid mechanism, the hormones or the the the proteins. If you have antibodies to that, then selenium can help drop that and lower that." (said at 0:22:12)

Both components of the claim are supported by published literature. First, iodothyronine deiodinases (the enzymes responsible for converting thyroxine [T4] to active triiodothyronine [T3]) are selenoproteins containing selenocysteine at their active site, making selenium essential for thyroid hormone activation. Second, systematic reviews and meta-analyses of randomized controlled trials demonstrate that selenium supplementation significantly reduces thyroid peroxidase autoantibody (TPOAb) titers in patients with Hashimoto's thyroiditis at 3- and 6-month follow-ups.

0:24:45Eric Berg (host)supportedmoderate

High doses of vitamin B2 (riboflavin) can successfully treat or manage migraines.

"Other people take high doses of vitamin B2 for migraines." (said at 0:24:45)

Randomized controlled trials and meta-analyses support the use of high-dose vitamin B2 (riboflavin, typically 400 mg daily) for migraine prophylaxis. A 2022 systematic review and meta-analysis of 9 clinical studies found that 400 mg/day of riboflavin for three months significantly reduced migraine attack frequency, duration, total migraine days, and pain severity compared to control groups.

0:28:40Eric Berg (host)supportedmoderate

Prednisone causes or contributes to leptin resistance.

"And even especially prednisone. Uh it can it's a synthetic version. It's a drug." (said at 0:28:40)

The host claims that prednisone (a synthetic glucocorticoid) causes or contributes to leptin resistance. This claim is supported by scientific evidence. Glucocorticoid administration (including synthetic corticosteroids such as prednisone and dexamethasone) markedly increases circulating leptin levels and impairs central and peripheral leptin signaling, inducing a state of leptin resistance. Clinical and preclinical studies show that glucocorticoid therapy induces hyperleptinemia and leads to central/hypothalamic leptin resistance, impairing leptin's ability to regulate appetite and energy expenditure (PMID: 37878899, PMID: 33045434, PMID: 24565674).

0:33:23Eric Berg (host)supportedmoderate

Consuming pure protein without sufficient fat or carbohydrates creates a dangerous metabolic imbalance because the human body can only use a limited amount of protein for fuel.

"That's why when you eat pure protein, it's actually very dangerous um because you you don't You can only use so much of that protein for fuel. It's Protein's used mainly for replacing body tissue and all the proteins and the chemistry and all that. So, we mainly get our fuel from fat and carbs. So, if you do this pure protein, we create a serious imbalance." (said at 0:33:23)

Human capacity to utilize protein as a primary fuel source is physiologically constrained by hepatic limits on amino acid deamination and urea synthesis to clear toxic nitrogenous waste. When dietary fat and carbohydrates are omitted and total energy needs are attempted to be met with pure protein, protein intake exceeds the metabolic ceiling (typically defined as >35% of energy intake or >285-365 g/day in an average adult), resulting in hyperaminoacidemia, hyperammonemia, nausea, diarrhea, and potentially fatal protein toxicity (known historically as 'rabbit starvation syndrome').

  • supports: A review of issues of dietary protein intake in humans. (International journal of sport nutrition and exercise metabolism 2006) · cited 228x in the literature
    "The key issues are the rate at which the gastrointestinal tract can absorb amino acids from dietary proteins (1.3 to 10 g/h) and the liver's capacity to deaminate proteins and produce urea for excretion of excess nitrogen. The accepted level of protein requirement of 0.8g x kg(-1) x d(-1) is based on structural requirements and ignores the use of protein for energy metabolism. High protein diets on the other hand advocate excessive levels of protein intake on the order of 200 to 400 g/d, which can equate to levels of approximately 5 g x kg(-1) x d(-1), which may exceed the liver's capacity to convert excess nitrogen to urea. Dangers of excessive protein, defined as when protein constitutes > 35% of total energy intake, include hyperaminoacidemia, hyperammonemia, hyperinsulinemia nausea, diarrhea, and even death (the "rabbit starvation syndrome")." (abstract, passage verified)
    pubmedfull study (doi)
0:34:08Eric Berg (host)supportedhigh

Insulin is a powerful sodium-retaining hormone in the body.

"It's true because insulin is a fat uh making hormone. It's help you store fat. It prevents you from burning fat, but it also has one of the most powerful sodium retainers." (said at 0:34:08)

Physiological and clinical research demonstrates that insulin acts directly on the kidneys to promote sodium reabsorption (an antinatriuretic effect). Human euglycemic-hyperinsulinemic clamp studies confirm that acute elevations in insulin stimulate distal tubular sodium reabsorption and decrease urinary sodium clearance. This sodium-retaining action is well-documented and remains preserved even in states of metabolic insulin resistance.

0:44:30Eric Berg (host)supportedhigh

Excessive intake of iodine temporarily shuts down or pauses biochemical reactions in the thyroid gland.

"there's a certain phenomena that occurs when you have excessive amounts of iodine. It's a protective mechanism because iodine is very rough on the body if you have too much of it. And so the body automatically shuts things down temporarily. It pauses biochemical reactions in the thyroid when you take too much iodine." (said at 0:44:30)

The speaker accurately describes the Wolff-Chaikoff effect, an established autoregulatory protective mechanism of the thyroid gland. When exposed to an acute excess of iodine or iodide, the thyroid gland rapidly and transiently inhibits intrathyroidal biochemical reactions—specifically iodide organification and thyroid hormone synthesis. Under normal physiological conditions, this shutdown is temporary; within several days, the thyroid gland downregulates the sodium-iodide symporter (NIS) to decrease intracellular iodide concentration and resumes normal hormone production (an adaptation known as 'escape' from the Wolff-Chaikoff effect).

0:50:45Eric Berg (host)supportedhigh

Fasting causes muscle breakdown rather than muscle building.

"and if you do prolonged fasting and you're postmenopausal and you are because you because your body if you when you do fasting, it's not building muscle. It's like breaking down muscle." (said at 0:50:45)

The claim that fasting results in net muscle protein breakdown rather than muscle building is supported by established human muscle physiology. In the fasted (postabsorptive) state, muscle protein breakdown exceeds muscle protein synthesis, resulting in a negative net muscle protein balance. Muscle protein synthesis requires exogenous amino acid availability and insulin stimulation from feeding to exceed breakdown and produce a positive net protein balance (hypertrophy/muscle building). Consequently, extended or prolonged fasting maintains a catabolic net protein state rather than an anabolic one.

0:54:50Eric Berg (host)supportedmoderate

It takes a time lag of 10 to 20 years for a person to progress from normal insulin function to overt diabetic abnormality.

"The time lag it takes for someone to go from normal to abnormal, and I'm talking mainly with insulin problems, is 10 to 15 to 20 years. So So that's how we're not connecting the dots very well because the real question is where are you on the spectrum of insulin damage?" (said at 0:54:50)

Longitudinal cohort studies evaluating the natural history and trajectory of type 2 diabetes demonstrate that metabolic derangements—particularly insulin resistance and compensatory hyperinsulinemia—develop and progress over a prolonged period of 10 to 15 or more years before overt clinical diabetes is diagnosed. In landmark prospective data from the Whitehall II study (Tabák et al., 2009), insulin sensitivity began declining over a decade before diagnosis (tracked up to 13 years prior), with compensatory beta-cell secretion increasing until 3 to 4 years before diagnosis, followed by a rapid collapse in beta-cell compensation and an abrupt rise in glucose levels.

  • supports: Trajectories of glycaemia, insulin sensitivity, and insulin secretion before diagnosis of … (Lancet (London, England) 2009) · cited 902x in the literature
    "We assessed retrospective trajectories of fasting and 2-h postload glucose, homoeostasis model assessment (HOMA) insulin sensitivity, and HOMA beta-cell function from up to 13 years before diabetes diagnosis (diabetic group) or at the end of follow-up (non-diabetics)... In the diabetic group (801 measurements), a linear increase in fasting glucose was followed by a steep quadratic increase (from 5.79 mmol/L to 7.40 mmol/L) starting 3 years before diagnosis of diabetes... and HOMA insulin sensitivity decreased steeply during the 5 years before diagnosis (to 86.7%). HOMA beta-cell function increased between years 4 and 3 before diagnosis (from 85.0% to 92.6%) and then decreased until diagnosis (to 62.4%)." (abstract, results, passage verified)
    pubmedfull study (doi)
0:52:08Eric Berg (host)supportedhigh

Diamine oxidase (DAO) is an enzyme that helps counteract and break down histamine accumulation in the body.

"So, there's certain people that have a problem with histamines and it builds up. And um um and DAO is uh an enzyme that actually helps counter that." (said at 0:52:08)

The host's statement accurately reflects established physiological biochemistry regarding diamine oxidase (DAO). DAO is the primary extracellular enzyme responsible for the metabolism and degradation of ingested and accumulated histamine in the body, preventing excessive histamine buildup and maintaining physiological homeostasis. In individuals with DAO deficiency or reduced DAO activity, histamine can accumulate and lead to histamine intolerance (HIT), causing symptoms across multiple organ systems.

0:59:20Eric Berg (host)supportedmoderate

Research data indicates there is a microbial or pathogen-related component involved in osteoarthritis and joint inflammation.

"what's also interesting when we deal with inflammation in a in a joint, even osteo, there's data to that shows that there's even a microbial aspect to it. So, there's even a pathogen that's involved in it." (said at 0:59:20)

Published research demonstrates that microbial and pathogen-related factors contribute to osteoarthritis (OA) and joint inflammation. Research on the 'gut-joint axis' shows that gut microbiome dysbiosis and increased intestinal permeability release bacterial products such as lipopolysaccharide (LPS) into circulation, promoting systemic and intra-articular inflammation. Furthermore, 16S rRNA gene sequencing studies have detected bacterial DNA signatures and translocated microbial material within human and animal articular cartilage, synovial tissue, and synovial fluid, with distinct alterations in microbial composition and increased gram-negative bacterial markers observed in osteoarthritic joints compared to healthy controls.

1:03:57Eric Berg (host)supportedhigh

Kidney stone pain is primarily caused by the pressure of fluid backing up from a urine flow obstruction rather than rough edges of the stone cutting tissue.

"the stone is literally creating a blockage in your urine flow in your kidney and that pressure that backs up causes severe internal cramping that I've experienced... And it's not necessarily the the rough edges that are causing bleeding and things like that. That doesn't That's there's not a lot of nerve endings. It's really the the pressure of the fluid backing up." (said at 1:03:57)

The host's description accurately reflects the established pathophysiology of renal colic. Renal colic pain is primarily caused by acute urinary tract obstruction leading to increased hydrostatic pressure upstream, causing distension and stretching of the renal pelvis, calyces, or ureter, accompanied by local smooth muscle spasm (hyperperistalsis) mediated by prostaglandins and other inflammatory mediators. It is not caused by stone edges cutting or scratching nerve endings in the urothelium.

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.