HoldsUp

Dr. Eric Berg DC · 2026-07-10 · Eric Berg (host), Steve, Dominic

The Dr. Berg Show LIVE - July 10, 2026

46 research-tied claims examined: 6 contradicted 5 overstated 8 context 25 supported 2 unverified

8

Needs context

0:24:45Eric Berg (host)needs contextmoderate

Consuming a high-carbohydrate breakfast causes a rapid spike in blood sugar followed by insulin-driven hypoglycemia that induces hunger shortly after eating.

"when you do that, you got this high sugar that comes up, but guess what? It's going to come right back down because of the insulin that's going to be spiked out there. So, it's going to push it down. And as soon as that comes down, you're going to have what's called low blood sugars. And then what that's going to create is something called hunger." (said at 0:24:45)

The speaker describes the classic 'glucostatic' or reactive hypoglycemia hypothesis: that a high-carbohydrate/high-glycemic meal triggers an insulin surge that drops glucose levels below baseline, subsequently driving hunger shortly afterward. While large-scale continuous glucose monitoring studies confirm that postprandial glucose dips (relative to baseline 2–3 hours post-meal) predict increased hunger, shorter latency to the next meal, and higher subsequent energy intake, the physiological phenomenon in healthy adults is typically a transient dip or return toward baseline rather than clinical hypoglycemia. Furthermore, trials assessing mixed meals and appetite show that postprandial satiety and appetite regulation are complex and mediated by multiple neurohormonal factors beyond glucose and insulin dynamics alone.

0:30:48Eric Berg (host)needs contextmoderate

Exercise, cold therapy, sauna, niacin (vitamin B3), and a low-carbohydrate diet increase mitochondrial biogenesis, whereas refined sugars and starches destroy mitochondria.

"One way to increase—it's called mitochondrial biogenesis—if you want to increase that, there's several things you can do. The top thing is called exercise... you have exercise, you have cold therapy. Yeah, cold therapy, even sauna, certain um nutrients can help support the mitochondria, especially niacin, B3. Um so there's a there's a low carb diet can help support the mitochondria. High refined sugars and starches destroy the mitochondria." (said at 0:30:48)

The speaker accurately identifies key physiological stimuli and nutrients that enhance mitochondrial biogenesis and function, though claiming that refined sugars and starches 'destroy' mitochondria is colloquial and hyperbolic for chronic metabolic overload and mitochondrial dysfunction. Clinical and mechanistic evidence confirms that physical exercise is a primary activator of the AMPK/SIRT1/PGC-1α axis to stimulate mitochondrial biogenesis and quality control. In human clinical trials, niacin (vitamin B3) supplementation has been shown to increase systemic NAD+ levels and stimulate mitochondrial biogenesis in skeletal muscle. Conversely, excessive intake of refined carbohydrates promotes cellular stress, reactive oxygen species generation, and impaired mitochondrial respiratory capacity rather than immediate organelle destruction.

0:31:49Eric Berg (host)needs contextmoderate

In hypoglycemia, consuming refined sugar or starches elevates blood sugar temporarily but triggers an insulin spike that drives glucose back down, worsening the condition over time.

"So, you want me to eat sugar after my blood sugars go down to raise my blood glucose? Well, what caused it to go down? Well, insulin. Okay. Well, what caused insulin to spike? Sugar, refined carbs. So, you want me to keep doing the thing that caused it? Like, explain how that makes common sense. Um, yes, you will elevate blood sugars by taking sugar or a starch or whatever or even eating, but the problem is you'll you'll make it worse over time." (said at 0:31:49)

The host's argument conflates the immediate clinical management of acute hypoglycemia with the dietary management of postprandial reactive hypoglycemia. For acute hypoglycemic episodes, clinical guidelines establish that consuming fast-acting simple carbohydrates (such as glucose or refined sugars) is the required, standard acute treatment to rapidly restore blood glucose levels to safe thresholds. However, in the context of postprandial reactive hypoglycemia (and post-bariatric/post-gastrectomy dumping syndrome), literature confirms that consuming high-sugar or high-carbohydrate meals triggers an exaggerated insulin response (hyperinsulinemia), which leads to subsequent rapid drops in blood glucose (rebound hypoglycemia). Evidence demonstrates that high-sugar intake elicits hypoglycemic episodes, whereas dietary management relying on low-carbohydrate, low-glycemic-index meals or low-carbohydrate enteral formulas stabilizes postprandial blood glucose and insulin levels.

0:37:08Eric Berg (host)needs contexthigh

Addison's disease is an autoimmune condition characterized by low cortisol, weight loss, skin hyperpigmentation, poor immune function, and inability to retain sodium.

"there's even a condition called Addison's, which you don't I don't think you have, so I wouldn't worry about that. But that's an autoimmune where you have low cortisol and you lose weight, and you actually your skin becomes a little bit darker, and then you have a poor immune system... in which case you have to actually consume more salt. So the question is, do you get more energy with salt? Because without that cortisol, you can't hold the salt." (said at 0:37:08)

The clinical presentation described is largely accurate: primary adrenal insufficiency (Addison's disease) is most commonly an autoimmune condition characterized by low cortisol, weight loss, skin hyperpigmentation, and sodium loss leading to salt craving. However, two aspects require qualification. First, the inability to retain sodium (salt wasting) is primarily caused by a deficiency of aldosterone (a mineralocorticoid produced by the adrenal cortex), rather than cortisol deficiency. Second, Addison's disease is caused by an autoimmune reaction (targeted immune destruction of adrenal cortical cells), not by an immunodeficient or 'poor' immune system.

0:54:09Eric Berg (host)needs contextmoderate

Egg yolks and liver are the highest dietary sources of choline, and choline acts to remove fat from the liver to prevent or reverse fatty liver disease.

"out of all the foods that have the most choline, liver is number one, egg yolks number two. So the egg yolk has a tremendous amount of choline. Choline specifically has the ability to remove fat from your liver. So, this is why eggs are really good for preventing or even reversing part of the fatty liver in conjunction with a low-carb diet." (said at 0:54:09)

The speaker accurately describes the biochemical role and primary dietary sources of choline, but extends these mechanisms to clinical claims about reversing non-alcoholic fatty liver disease (NAFLD) with eggs that require qualification. Beef liver and egg yolks are among the richest dietary sources of choline. Biochemically, choline is an essential precursor for phosphatidylcholine, which is required for the assembly and secretion of very-low-density lipoproteins (VLDL) that export triglycerides out of hepatocytes. Choline deficiency reliably induces hepatic steatosis in humans and animal models, and higher total dietary choline intake is observationally associated with reduced NAFLD risk. However, direct evidence from randomized trials demonstrating that consuming whole eggs reverses clinical NAFLD is lacking, and large prospective cohort studies (such as the Framingham Heart Study) found that while total dietary choline was inversely associated with NAFLD risk, egg consumption itself was not directly associated with reduced NAFLD incidence or changes in liver fat.

1:01:50Eric Berg (host)needs contexthigh

The Recommended Dietary Allowance (RDA) for magnesium is between 380 and 420 milligrams.

"the RDA for magnesium is like between 380 and 420" (said at 1:01:50)

The Recommended Dietary Allowance (RDA) for magnesium established by the Institute of Medicine (National Academies) varies by sex and age. For adult men, the RDA is 400 mg/day (ages 19-30) and 420 mg/day (ages 31 and older), which aligns closely with the stated range of 380 to 420 mg. However, for adult women, the RDA is lower at 310 mg/day (ages 19-30) and 320 mg/day (ages 31 and older), rising to 350-360 mg/day during pregnancy. Across the entire adult population, the RDA ranges from 310 to 420 mg/day.

1:03:22Eric Berg (host)needs contextlow

Consuming fewer carbohydrates reduces cyst formation, while consuming more sugar and alcohol increases cyst growth.

"the lower the carbohydrate, the less cysts that people have. In practice, I've just observed that they start growing more cysts if they're consuming more sugar, even alcohol as well." (said at 1:03:22)

The claim is partially supported by clinical and preclinical research in polycystic kidney disease (ADPKD), but it overstates the evidence as general clinical truth or established practice observation rather than preliminary findings. Preclinical research and early clinical trials show that ketogenic interventions (low-carbohydrate diets, periodic fasting, or beta-hydroxybutyrate supplementation) reduce cyst burden, slow kidney growth, and improve renal function in ADPKD. Polycystic kidney cells rely on glycolysis for energy, so carbohydrate restriction deprives them of glucose and induces ketosis, which inhibits cyst expansion. In an exploratory randomized controlled trial (KETO-ADPKD), a ketogenic diet reduced body fat and liver volume with a non-statistically significant reduction in kidney volume, while improving kidney function compared to controls. Retrospective case series and observational cohorts also document stabilization or reduction of total kidney volume during low-carbohydrate/ketogenic therapies. However, specific evidence directly linking sugar or alcohol intake per se to accelerated cyst growth in humans remains limited primarily to mechanism-based models and real-world case reports/expert observation, rather than definitive epidemiologic or trial evidence.

1:03:54Eric Berg (host)needs contextmoderate

Shiitake and other mushrooms build up white blood cells.

"Shiitake mushroom, other mushrooms are great to build up the white blood cells." (said at 1:03:54)

Dietary consumption of shiitake mushrooms (Lentinula edodes) and mushroom-derived extracts has been shown in human and animal trials to stimulate the proliferation, activation, and function of specific white blood cell subsets (notably γδ-T cells, natural killer T cells, and cytotoxic lymphocytes). However, describing this as 'building up white blood cells' is a colloquial oversimplification: mushrooms do not simply elevate total circulating leukocyte counts in healthy individuals, but rather modulate immune cell activity, proliferation capacity, and cytokine responses.

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.