HoldsUp

Andrew Koutnik

Andrew Koutnik is a researcher in the fields of nutrition, exercise physiology, and metabolism. His published research focuses on the effects of carbohydrate intake, exogenous ketone supplementation, and ketogenic diets on exercise performance, metabolism, and cognitive function. Additionally, his work investigates the physiological and cardiovascular impacts of nutritional interventions in individuals with type 1 diabetes.

42 claims checked on air: 5 context 1 contradicted 2 overstated 25 supported 9 unverified

What they said on air - context

4 citing their own research

0:00:00needs contextmoderateThe Fuel Myth: Rethinking Carbs, Brain Health, and Human Per

Athletes following a ketogenic diet did not experience deterioration in physical performance compared to those on a high-carbohydrate diet.

"What we found is that when athletes were either on a ketogenic diet or on a high carb diet, the ketogenic diet did not produce any deterioration in physical performance." (said at 0:00:00)

The claim that a ketogenic diet causes no deterioration in athletic performance compared to a high-carbohydrate diet requires important qualification. Systematic reviews and position stands show that the impact of a ketogenic diet is highly dependent on exercise intensity, duration, and adaptation time. For maximal strength, resistance training, and moderate-intensity endurance (such as VO2 max and time to exhaustion), evidence indicates performance is generally preserved compared to high-carbohydrate diets. However, for high-intensity endurance, exercise economy, and elite-level competition, ketogenic diets frequently result in performance decrements or reduced efficiency compared to carbohydrate-rich diets.

0:25:30needs contextmoderatetheir own paperThe Fuel Myth: Rethinking Carbs, Brain Health, and Human Per

Administration of exogenous ketones without dietary changes improves cognitive retention during acute hypoxic exposure at altitudes between 15,000 and 20,000 feet.

"we've studied just the mere application of ketones independent of diet change and see profound effects in various conditions, including in extreme environments like high altitude hypoxic exposure for special operations command grant looking at the ability to improve resilience against hypoxia exposure. Anywhere between 15 to 20,000 foot altitude immediate exposure and it increased the ability to have retained cognition in these extreme environments." (said at 0:25:30)

Exogenous ketone supplementation (such as ketone monoesters) taken acutely without dietary changes has been shown in controlled laboratory studies to partially attenuate declines in specific cognitive and psychomotor functions—such as reaction time on vigilance tests and code substitution performance—during severe acute hypoxic exposure simulating altitudes of 15,000 to 20,000 feet (4,500 to 6,100 m). However, the evidence is domain-specific and mixed: several randomized trials have found that while exogenous ketones improve blood oxygen saturation or neural signaling under hypoxia, they do not consistently improve broader cognitive test batteries, complex task performance, or real-world field performance during high-altitude operations.

0:40:35needs contextvery lowThe Fuel Myth: Rethinking Carbs, Brain Health, and Human Per

Beta-hydroxybutyrate alters epigenetic gene expression through beta-hydroxybutyrylation and activates FOXO antioxidant genes.

"There's actually something called beta-hydroxybutyrylation, which is an epigenetic change... And one of those genes is is a FOXO gene, which specifically is an antioxidant-producing gene, which so as a way of actually causing anti or scavenging oxidative stress molecules." (said at 0:40:35)

Beta-hydroxybutyrate (βOHB) acts as an epigenetic regulator via both histone deacetylase (HDAC) inhibition and lysine beta-hydroxybutyrylation. In cellular and rodent models, βOHB increases histone acetylation at the Foxo3a promoter (via class I HDAC inhibition), upregulating FOXO3A transcription and conferring protection against oxidative stress. FOXO3A is a transcription factor that upregulates antioxidant enzymes (such as superoxide dismutase and catalase) rather than directly producing antioxidant molecules. While the speaker conflates beta-hydroxybutyrylation with the HDAC-inhibition-driven histone acetylation mechanism originally demonstrated for FOXO activation, βOHB is an established epigenetic regulator that enhances FOXO-mediated antioxidant pathways in preclinical models.

0:54:05needs contexthighThe Fuel Myth: Rethinking Carbs, Brain Health, and Human Per

In the 1960s, Jonas Bergström developed the percutaneous muscle biopsy technique and showed that glucose is stored in muscle as glycogen.

"It wasn't until the 1960s where a physician named Jonas Bergström discovered the ability to actually stick a syringe into the muscle and do something called a muscle biopsy, so, they called the Bergström muscle biopsy, where they actually suctioned out a piece of muscle. And what they were finding is, oh wow, lo and behold, when we pull out muscle and analyze that muscle tissue, glucose was being stored as something called glycogen." (said at 0:54:05)

The speaker accurately describes Jonas Bergström's introduction of the percutaneous needle muscle biopsy technique in the 1960s, which used a specialized needle and suction to obtain skeletal muscle samples in humans, revolutionizing the study of human exercise physiology and glycogen dynamics in vivo. However, the claim that this led to the initial discovery that glucose is stored in muscle as glycogen is historically inaccurate; glycogen and its role as a stored carbohydrate in liver and muscle had been established more than a century earlier (initially isolated by Claude Bernard in the 1850s and extensively characterized in muscle throughout the early 20th century). Bergström and colleagues used the biopsy technique to demonstrate how human muscle glycogen content fluctuates, depleting during exercise and supercompensating with dietary carbohydrate.

1:03:34needs contexthighThe Fuel Myth: Rethinking Carbs, Brain Health, and Human Per

In the medical literature, 70 mg/dL (3.9 mmol/L) is typically defined as the threshold for hypoglycemia because the majority of individuals experience symptoms at or below that level.

"in the medical literature 70 mg/dL or 3.9 mmol is usually the threshold for hypoglycemia. Why is it used as a threshold for hypoglycemia? Because the vast majority of people will experience symptoms at or below that level." (said at 1:03:34)

While 70 mg/dL (3.9 mmol/L) is widely established in clinical practice guidelines and consensus statements as the alert threshold for hypoglycemia, the physiological rationale given is inaccurate. Experimental clamp studies establishing the hierarchy of glycemic thresholds show that autonomic counterregulatory hormones (epinephrine, glucagon) begin to release at approximately 65–68 mg/dL, whereas autonomic symptoms (such as sweating, tremor, and palpitations) do not typically occur until glucose drops to approximately 55–58 mg/dL (and neuroglycopenic symptoms below ~50 mg/dL). The 70 mg/dL cutoff is selected as a safety threshold because it approximates the upper limit of physiological counterregulation, providing an early margin of safety to prevent symptomatic or neuroglycopenic hypoglycemia, rather than because symptoms occur at 70 mg/dL.

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