The notion that low-carb diets cause undue stress on the body through excessive gluconeogenesis—the process by which the liver and kidneys produce glucose from non-carbohydrate sources—has been a persistent myth. Critics argue that low-carb diets, by reducing glucose intake, force the body into a state of heightened gluconeogenesis, taxing organs and elevating stress hormones like cortisol. However, well-designed trials and physiological evidence debunk this claim, showing that gluconeogenesis is a normal, regulated process that occurs regardless of dietary carbohydrate levels.
Gluconeogenesis is an essential metabolic pathway, active even in high-carb diets, as the body must maintain stable blood glucose for tissues like the brain and red blood cells. Studies, such as those published in The American Journal of Clinical Nutrition (e.g., Bisschop et al., 2000), demonstrate that gluconeogenesis contributes significantly to glucose production in both fed and fasted states, with rates varying little between high- and low-carb diets. In low-carb settings, the body efficiently shifts to using substrates like glycerol from fat breakdown and amino acids from protein, without evidence of metabolic strain.
Trials like those by Gannon and Nuttall (2004) further show that low-carb diets do not significantly elevate cortisol or other stress markers compared to high-carb diets, as gluconeogenesis is tightly regulated by insulin, glucagon, and substrate availability. The body adapts by increasing ketone production for energy, reducing reliance on glucose and thus gluconeogenesis over time. Far from stressing the body, this metabolic flexibility is a hallmark of human physiology.
The myth likely stems from misunderstanding gluconeogenesis as an emergency response rather than a routine process. With no consistent evidence linking low-carb-induced gluconeogenesis to organ stress or hormonal imbalance, the claim fails to hold up. Low-carb diets, when well-formulated, support metabolic health without overburdening this natural pathway.
