HoldsUp

Dr. Eric Berg DC · 2026-07-24 · Eric Berg (host), Steve, Jeff, Kathy Everett

The Dr. Berg Show LIVE - July 24, 2026

50 research-tied claims examined: 3 contradicted 8 overstated 7 context 26 supported 6 unverified

26

Supported by research

0:06:56Eric Berg (host)supportedmoderate

Breaking a prolonged fast with sugar causes a dangerous shift in potassium levels.

"Now, especially if you're getting into prolonged fasting, very dangerous to break your fast with sugar because it creates a huge shift in potassium and it makes this body shift and it creates a dangerous situation." (said at 0:06:56)

Breaking a prolonged fast (typically considered >5 days of minimal or no caloric intake) with rapid carbohydrate or sugar intake triggers a surge in insulin secretion. Insulin stimulates the cellular uptake of glucose along with potassium, phosphate, and magnesium via the Na+/K+-ATPase and other transporters. This rapid intracellular shift can precipitate acute hypokalemia, hypophosphatemia, and hypomagnesemia (hallmarks of refeeding syndrome), which can lead to life-threatening cardiac arrhythmias, neuromuscular dysfunction, and sudden death.

0:10:22Eric Berg (host)supportedhigh

Getting bright sunlight in the morning for 10 to 30 minutes resets your circadian rhythm.

"mainly you want to have bright sunlight in the morning for at least 10 to 15 to 20 to 30 minutes as more the better in the morning. That resets your circadian rhythm at night." (said at 0:10:22)

Light is the primary environmental cue (zeitgeber) that synchronizes and entrains the human circadian pacemaker. Exposure to bright light in the morning produces a phase advance—shifting the circadian rhythm and the onset of nocturnal melatonin earlier. Human chronobiology studies confirm that bright, blue-enriched light exposure in the morning, including natural sunlight, resets circadian timing, with measurable phase advances achievable even within short exposure durations and single circadian cycles.

0:13:33Eric Berg (host)supportedlow

Muscle relaxation is mediated by a magnesium-fueled pump that pumps calcium out of the cell, and magnesium deficiency impairs this pump, resulting in muscle twitches, cramps, and jaw clenching.

"What happens, calcium goes in, causes contraction. Then there's something that triggers a nerve that triggers the uh the exit of that calcium out which is then controlled by a little pump which is fueled by magnesium. So if you don't have enough magnesium that pump can't work and you tend to get more contraction problems, uh muscle twitches, leg cramps, feet cramps in the middle of the night and even your jaw tends to be tight." (said at 0:13:33)

Muscle contraction is initiated by an increase in intracellular calcium, while muscle relaxation relies on calcium extrusion and sequestration by ATP- and magnesium-dependent calcium pumps (such as the plasma membrane Ca2+-ATPase and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). In addition, clinical magnesium deficiency (hypomagnesemia) is established to cause neuromuscular irritability, presenting with symptoms such as muscle fasciculations (twitches), diffuse cramps, and muscle spasms.

0:18:57Eric Berg (host)supportedhigh

Cholesterol is required to build cell membranes, synthesize steroid hormones, make vitamin D, and produce bile salts.

"So, think about our bodies make cholesterol. Why? For these things called cell membranes, right? To keep everything working. It's really those cell membranes are super important also to make hormones. A lot of your hormones are made from cholesterol. You can't make vitamin D without cholesterol. You can't make bile salts without cholesterol." (said at 0:18:57)

The host's statement accurately summarizes well-established physiological facts regarding cholesterol. Published biological and physiological literature confirms that cholesterol is an essential component of cell membranes (regulating membrane structure and fluidity) and serves as the fundamental precursor for the synthesis of all steroid hormones, vitamin D (7-dehydrocholesterol), and bile acids/salts.

0:20:45Eric Berg (host)supportedhigh

Selenium is vital for the enzymatic conversion of thyroid hormone T4 to T3.

"So many people have a thyroid problem, but the the real problem is is the conversion from T4 to T3 because they don't have enough selenium. Selenium is vital for that conversion." (said at 0:20:45)

Selenium is an essential constituent of the iodothyronine deiodinase enzymes (DIO1 and DIO2), which are selenoproteins containing selenocysteine at their catalytic sites. These enzymes are directly responsible for the enzymatic conversion of the prohormone thyroxine (T4) to active triiodothyronine (T3). Severe selenium deficiency impairs deiodinase activity, leading to alterations in the T4 to T3 ratio, which normalize upon selenium repletion.

0:28:41Eric Berg (host)supportedhigh

The human body lacks an active physiological mechanism to excrete excess iron.

"Yeah, our body doesn't really have any way of getting rid of excess iron. So, you're going to have to go to a get a prescription to donate blood or I think you could just go and donate blood every couple months and uh and get rid of that excess iron." (said at 0:28:41)

The claim is supported by established physiological consensus. Unlike many other minerals and electrolytes, the human body lacks an active, regulated physiological mechanism for iron excretion. Systemic iron balance is regulated almost entirely at the level of intestinal iron absorption (governed by hepcidin, ferroportin, and DMT1). Basal iron loss occurs only passively and at a low rate through skin exfoliation, shedding of intestinal epithelial cells, and minor blood loss. Because there is no active pathway to excrete excess iron once absorbed, conditions of iron overload require external removal methods such as phlebotomy (blood donation) or iron chelation therapy.

0:15:13Eric Berg (host)supportedmoderate

Unexplained easy bruising in young individuals can be caused by a vitamin C deficiency or a vitamin K1 deficiency.

"and you're younger and you still get this bruising easily. that that would be either um a vitamin C deficiency or a vitamin K1 deficiency" (said at 0:15:13)

Both vitamin C deficiency (scurvy) and vitamin K deficiency are recognized medical causes of easy bruising and skin bleeding manifestations (such as petechiae and ecchymoses), including in younger patients and children. Severe vitamin C deficiency impairs collagen synthesis, causing capillary fragility that manifests as easy bruising, petechiae, and ecchymoses. Vitamin K deficiency leads to impaired carboxylation of vitamin K-dependent clotting factors (factors II, VII, IX, and X), resulting in coagulopathy and cutaneous bleeding/bruising. While other etiologies such as immune thrombocytopenia or platelet dysfunction are also part of the differential diagnosis for unexplained easy bruising, nutritional deficiencies of vitamin C and vitamin K are established causes.

0:19:47Eric Berg (host)supportedhigh

In addition to T4, the thyroid gland produces calcitonin and triiodothyronine (T3).

"the thyroid produces more than T4 it produces uh calcitonin that's another compound on it. And there's other things, a little bit of T3, too." (said at 0:19:47)

Established endocrine physiology confirms that the thyroid gland produces hormones beyond thyroxine (T4). Specifically, the thyroid follicular cells synthesize and secrete both T4 and a smaller proportion of triiodothyronine (T3, with the majority of circulating T3 subsequently generated via peripheral deiodination of T4), while the parafollicular cells (C cells) of the thyroid gland synthesize and secrete the peptide hormone calcitonin.

0:26:40Eric Berg (host)supportedmoderate

The coronary artery calcification (CAC) score is a strong predictor of mortality.

"Another test would be the CAC test, coronary artery calcification test, because that will tell you uh, you know, your score, and you don't want it really high because that's a good predictor of mortality." (said at 0:26:40)

Large systematic reviews and meta-analyses of prospective and retrospective cohort studies demonstrate that higher coronary artery calcium (CAC) scores strongly predict all-cause and cardiovascular mortality in both asymptomatic individuals and symptomatic patients without established coronary artery disease.

0:30:56Eric Berg (host)supportedhigh

Excessive selenium intake can cause hair loss and brittle nails.

"Yes, you could take too much selenium and then get hair loss and brittle nails." (said at 0:30:56)

Excessive selenium intake (selenosis) is well-established to cause hair loss (alopecia) as well as brittle, dystrophic nails or nail loss. These dermatologic and appendage manifestations are hallmark clinical signs of both acute and chronic selenium toxicity in humans.

0:32:48Eric Berg (host)supportedvery low

Vitamin D decreases estrogen receptor sensitivity and expression.

"vitamin D helps to decrease the sensitivity of the receptor for estrogen." (said at 0:32:48)

Preclinical studies show that the active form of vitamin D (1,25-dihydroxyvitamin D3 or calcitriol) directly down-regulates estrogen receptor alpha (ERα) gene transcription and protein expression in estrogen-responsive cells (such as MCF-7 breast cancer cells), attenuating estrogen receptor signaling and sensitivity to estradiol-stimulated bioresponses. However, this evidence is derived entirely from in vitro and animal models, and clinical evidence in humans remains preliminary.

0:36:14Eric Berg (host)supportedhigh

Dietary soluble fiber lowers blood cholesterol by binding bile salts in the gut rather than directly binding cholesterol.

"A lot of people are doing uh psyllium husk fiber and oat fiber and uh flax fiber and all these things and they think it's connecting to cholesterol and pulling it out. It's not. It's not how it works at all. What it does is it binds to your bile salts. Your bile salts. The bile pathways are the primary mode of getting rid of excess cholesterol. So, if you're going to bind up a lot of your bile, um, guess what? You then cause this overreaction of your body making more bile to deal with the cholesterol." (said at 0:36:14)

The host's statement that dietary soluble fiber (such as psyllium, oat, or flax fiber) lowers blood cholesterol primarily by binding bile salts/acids in the gut to enhance their fecal excretion (which forces the liver to synthesize new bile acids from hepatic cholesterol) rather than directly binding cholesterol itself is accurate and well-supported by scientific evidence. Soluble fibers trap or bind bile acids in the intestine and prevent their enterohepatic reabsorption, leading to upregulation of hepatic bile acid synthesis via 7α-hydroxylase (CYP7A1) and an increase in hepatic LDL receptor activity to clear LDL cholesterol from the blood.

0:39:22Eric Berg (host)supportedhigh

Zinc carnosine heals gastritis and gastric ulcers, including ulcers caused by NSAIDs.

"There's a really uh simple and great, effective thing for gastritis and ulcers, uh especially if you got that from taking an NSAID um medication, and it's called zinc carnosine. Okay? Goes in there, it helps heal the ulcer" (said at 0:39:22)

Zinc carnosine (also known as polaprezinc or zinc L-carnosine) is a mucosal protective agent approved and prescribed in countries such as Japan and China for the treatment of gastric ulcers and gastritis. Randomized controlled trials and clinical reviews demonstrate that zinc carnosine promotes mucosal healing, protects against mucosal injury (including damage from NSAIDs and H. pylori gastritis), and accelerates the endoscopic resolution of gastric ulcers.

0:49:23Eric Berg (host)supportedhigh

Estrogen in the female body is synthesized from testosterone.

"and even having enough testosterone, because your estrogen in a female comes from testosterone." (said at 0:49:23)

Estrogen biosynthesis in the female body relies directly on androgen precursors. The enzyme aromatase (encoded by CYP19A1) catalyzes the aromatization of C19 androgens into estrogens—specifically converting testosterone into estradiol (E2) and androstenedione into estrone (E1) in both the ovaries and peripheral tissues (such as adipose tissue, brain, and bone).

0:56:58Eric Berg (host)supportedvery low

Magnesium acetyl taurate crosses the blood-brain barrier.

"There's another version I like better and it might not be as expensive. It's called magnesium acetyl taurate. That version definitely crosses the blood-brain barrier." (said at 0:56:58)

Preclinical animal pharmacokinetic studies demonstrate that magnesium acetyl taurate crosses the blood-brain barrier and increases magnesium concentrations in brain tissue and cerebrospinal fluid more effectively than several other common magnesium formulations. However, direct human evidence evaluating central nervous system penetration remains limited, restricting the certainty of the body of evidence to very low due to reliance on rodent models.

0:56:41Eric Berg (host)supportedmoderate

L-theanine crosses the blood-brain barrier.

"L-theanine actually has this unique—it's not based on a lot of studies. I think it might be one study, but it does cross the blood-brain barrier." (said at 0:56:41)

Preclinical pharmacokinetic and neurochemical studies demonstrate that L-theanine readily crosses the blood-brain barrier, primarily via the leucine-preferring amino acid transport system (System L).

0:59:12Eric Berg (host)supportedmoderate

Scientific research shows that increasing magnesium intake reduces the occurrence of migraine headaches.

"There's a lot of data on more magnesium, less headaches, especially migraine headaches, because you think about like you have all these spasmodic contractions and vasoconstrictions and things like that that magnesium can help normalize that." (said at 0:59:12)

Multiple systematic reviews and meta-analyses of randomized controlled trials indicate that oral magnesium supplementation reduces migraine attack frequency, severity, and monthly migraine days compared to placebo. While some individual trials have mixed results and varying methodological quality, pooled analyses consistently demonstrate a beneficial effect for migraine prophylaxis.

1:01:47Eric Berg (host)supportedlow

Applying onion juice helps treat a specific type of hair loss, supported by research.

"The onion video that I did helped a certain type of hair loss. There's a study on it. It's pretty credible." (said at 1:01:47)

A small single-blinded controlled clinical trial published in 2002 evaluated the application of crude onion juice (Allium cepa L.) twice daily in patients with patchy alopecia areata. Hair regrowth was observed in 86.9% (20/23) of patients in the onion juice group at six weeks, compared to 13.3% (2/15) in the tap-water control group (P < 0.0001). However, the evidence certainty remains low due to small sample size, lack of double-blinding (given the distinct odor of onion juice), and the absence of larger confirmatory trials.

  • supports: Onion juice (Allium cepa L.), a new topical treatment for alopecia areata. (The Journal of dermatology 2002) · cited 99x in the literature
    "At four weeks, hair re-growth was seen in 17 patients (73.9%), and, at six weeks, the hair re-growth was observed in 20 patients (86.9%) and was significantly higher among males (93.7%) compared to females (71.4%) P<0.0001. In the tap-water treated-control group, hair re-growth was apparent in only 2 patients (13%) at 8 weeks of treatment with no sex difference. The present study showed that the use of crude onion juice gave significantly higher results with regard to hair re-growth than did tap water (P<0.0001), and that it can be an effective topical therapy for patchy alopecia areata." (abstract, results, passage verified)
    pubmedfull study (doi)
1:01:57Eric Berg (host)supportedmoderate

Hair loss can be caused by vitamin D deficiency, protein deficiency, mineral deficiencies, or elevated DHT.

"you can have a nutrient deficiency and multiple nutrients. You could have a mineral deficiency, you could have a vitamin D deficiency, you could have a protein deficiency, you could have high DHT. There's a lot of different factors." (said at 1:01:57)

Hair loss (alopecia and telogen effluvium) is multifactorial and has well-documented associations with nutritional and hormonal imbalances. Dihydrotestosterone (DHT) is established as a key androgen driving androgenetic alopecia. In addition, systematic reviews of clinical and observational evidence indicate that micronutrient deficiencies—including vitamin D and essential minerals such as iron and zinc—as well as macronutrient insufficiency play significant roles in disrupting the normal hair follicle cycle and hair growth.

1:03:08Eric Berg (host)supportedmoderate

Vitamin A deficiency can cause dry eyes and dry mouth.

"But typically dry eyes and even dry mouth can come from a vitamin A deficiency." (said at 1:03:08)

Vitamin A is essential for the maintenance and differentiation of specialized epithelial tissues, including the ocular surface and oral mucosa. Vitamin A deficiency classically causes xerophthalmia (abnormal dryness of the conjunctiva and cornea) and can lead to mucosal keratinization defects resulting in xerostomia (dry mouth).

1:03:15Eric Berg (host)supportedmoderate

Vitamin A will not work effectively in the body if a person is deficient in zinc.

"But then again, vitamin A won't work if you're deficient in zinc." (said at 1:03:15)

Zinc plays an essential role in vitamin A metabolism, mobilization, and function. Zinc is required for the hepatic synthesis and secretion of retinol-binding protein (RBP), the primary transport protein that carries retinol from liver stores to target tissues. In addition, zinc is a crucial cofactor for zinc-dependent enzymes in vitamin A metabolism, such as retinol dehydrogenase, which converts retinol to retinal in the visual cycle. Clinical trials show that zinc deficiency impairs vitamin A bioavailability and that co-supplementation with zinc and vitamin A is significantly more effective at correcting vitamin A deficiency than vitamin A supplementation alone.

1:04:38Eric Berg (host)supportedmoderate

Postmenopausal women experience anabolic resistance, where muscle tissue resists signals for growth and synthesis.

"And that related to women after menopause, they're trying to get their muscle back. They look—it looks like they have cellulite. Like, what's going on? And they try to work out, and then they try to have more protein or they add more hormones, and like nothing's working. It's a really interesting thing, because they have what's called anabolic resistance. That muscle is ignoring the signals." (said at 1:04:38)

Published human physiological studies demonstrate that postmenopausal and older women exhibit anabolic resistance. Anabolic resistance is defined as a blunted or refractory muscle protein synthesis (MPS) response to fundamental anabolic stimuli, including dietary protein/essential amino acid ingestion and resistance exercise, mediated by impaired downstream anabolic signaling (such as the mTOR pathway).

1:05:08Eric Berg (host)supportedhigh

Resistance training opens an uptake window for dietary protein in muscle tissue for 24 hours post-workout.

"The muscle then opens a door, a back door for the protein for 24 hours after that workout where they can now deliver protein from animal protein meat." (said at 1:05:08)

Randomized physiological tracer studies show that a bout of resistance exercise increases skeletal muscle sensitivity to amino acid intake and enhances myofibrillar protein synthesis in response to protein feeding for at least 24 hours (and up to 24–48 hours) post-workout, rather than being restricted to a narrow immediate post-exercise window.

1:05:27Eric Berg (host)supportedhigh

Leucine triggers muscle growth signaling.

"So that leucine, that's an amino acid, tells the muscle to start growing, especially after the door is open from the exercise." (said at 1:05:27)

Extensive human and preclinical research confirms that the essential branched-chain amino acid leucine acts as a primary nutrient trigger for skeletal muscle growth signaling. Leucine directly activates the mechanistic target of rapamycin complex 1 (mTORC1) pathway—specifically phosphorylating downstream targets such as p70S6K and 4E-BP1 that regulate translation initiation and muscle protein synthesis. Furthermore, prior resistance exercise sensitizes skeletal muscle to leucine and amino acid signaling, synergistically augmenting post-exercise muscle protein synthesis rates.

1:05:49Eric Berg (host)supportedhigh

Age-related muscle loss is called sarcopenia.

"prevent age-related muscle loss, which is called sarcopenia." (said at 1:05:49)

The host's statement accurately reflects the established medical definition. Sarcopenia is defined internationally as the progressive, age-related loss of muscle mass, strength, and function.

1:04:28Eric Berg (host)supportedhigh

Whey protein contains the highest concentration of the amino acid leucine among dietary protein sources.

"whey protein also has the most leucine, but even parmesan cheese has leucine." (said at 1:04:28)

Whey protein contains approximately 11% to 13% leucine by weight of protein, which is the highest leucine concentration among commonly consumed dietary animal and plant protein sources (compared to casein at ~8–9%, egg at ~7–8%, and soy at ~6–8%). This high leucine density, combined with rapid digestion kinetics, makes whey particularly effective at triggering muscle protein synthesis.

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.