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Chapter 2 Why the Heart and Brain Use Ketones: Veech’s Thermodynamic Hypothesis and Its Limits
An apparent paradox
The previous chapter found that, per molecule of oxygen, ketones yield less ATP than glucose. Yet in some experiments a heart supplied with ketones as well as glucose did more work without a matching rise in oxygen use. Richard Veech and colleagues explained this with mitochondrial thermodynamics (Sato et al. 1995; Veech et al. 2001; Veech 2004). This chapter computes the argument with the Nernst equation and then asks how much evidence there is for it in humans.
Where the energy comes from: the redox span
The mitochondrial respiratory chain passes electrons from NADH to oxygen, pumping protons across the inner membrane along the way, and the protons flowing back drive ATP synthesis. The “head” of energy depends on the redox potential difference between electron donor and acceptor. The potential of a couple is given by the Nernst equation:
where is the number of electrons transferred and the Faraday constant. The free energy released when an electron pair moves from NADH to coenzyme Q is:
The free energy of ATP hydrolysis depends on the concentrations of ATP, ADP and inorganic phosphate:
Veech’s argument has two steps. First, ketone metabolism makes the free mitochondrial NAD couple more reduced (a higher NADH/NAD+ ratio) and the coenzyme Q couple more oxidised, widening the potential difference between them so that each electron pair can do more work. Second, in the perfused heart the measured free energy of ATP hydrolysis also became larger in magnitude (Sato et al. 1995; Veech 2004).
Note
How the Q couple is “seen”. In such experiments the redox state of the coenzyme Q couple is usually not measured directly but inferred from the ratio of succinate to fumarate in the tissue: succinate dehydrogenase (complex II) links the succinate/fumarate couple with the Q couple, and if it is assumed to be near equilibrium, the former can stand for the latter. The assumption is itself a link in the chain of inference, not a direct observation.
Calculation
The Nernst equation applied to two states. All concentration ratios are illustrative, chosen only to show the direction of the changes Veech and colleagues reported, not their measured values.
# Veech's thermodynamic argument, computed with the Nernst equation. Every concentration ratio below
# is ILLUSTRATIVE: chosen only to show the direction of change Veech and colleagues reported in the
# working perfused rat heart (Sato et al. 1995; Veech 2004), not their measured values.
# E = E0' - (R T / n F) ln([reduced]/[oxidised]) (n = 2 electrons)
# Delta G of the electron pair moved from NADH to coenzyme Q: dG = -n F (E_Q - E_NAD)
# Free energy of ATP hydrolysis: dG_ATP = dG0' + R T ln([ADP][Pi]/[ATP])
import math
R, T, F = 8.314, 310.15, 96485.0
RT = R * T / 1000 # kJ/mol
E0_NAD, E0_FUM = -0.320, 0.031 # volts at pH 7: NAD+/NADH and fumarate/succinate
# The Q couple is not measured directly in such experiments; it is commonly inferred from the
# fumarate/succinate ratio, on the assumption that succinate dehydrogenase (complex II) keeps the
# two couples close to equilibrium.
def E(E0, red_over_ox, n=2):
return E0 - (R * T / (n * F)) * math.log(red_over_ox)
def dG_ATP(atp_mM, adp_uM, pi_mM, dG0=-30.5):
return dG0 + RT * math.log((adp_uM * 1e-6) * (pi_mM * 1e-3) / (atp_mM * 1e-3))
states = { # mitochondrial free [NADH]/[NAD+], [succinate]/[fumarate], cytosolic free ADP (uM), Pi (mM)
"glucose only": dict(nadh_nad=0.05, succ_fum=1.5, adp=60, pi=3.0),
"glucose + ketones": dict(nadh_nad=0.15, succ_fum=0.7, adp=40, pi=1.5),
}
print("state E(NAD) mV E(Q, via fumarate) mV span mV dG of span kJ/mol dG_ATP kJ/mol")
for name, s in states.items():
e_nad = E(E0_NAD, s["nadh_nad"]); e_q = E(E0_FUM, s["succ_fum"])
span = e_q - e_nad
dg_span = -2 * F * span / 1000
g_atp = dG_ATP(8.0, s["adp"], s["pi"])
print(f"{name:18s} {e_nad * 1000:9.0f} {e_q * 1000:21.0f} {span * 1000:8.0f} {dg_span:18.1f} {g_atp:14.1f}")
print(f"each 10-fold change in [NADH]/[NAD+] moves E(NAD) by {R * T / (2 * F) * math.log(10) * 1000:.1f} mV")
print(f"each 10-fold change in [ADP][Pi] moves dG_ATP by {RT * math.log(10):.1f} kJ/mol")
# state E(NAD) mV E(Q, via fumarate) mV span mV dG of span kJ/mol dG_ATP kJ/mol
# glucose only -280 26 306 -59.0 -58.1
# glucose + ketones -295 36 330 -63.8 -60.9
# each 10-fold change in [NADH]/[NAD+] moves E(NAD) by 30.8 mV
# each 10-fold change in [ADP][Pi] moves dG_ATP by 5.9 kJ/molIn these illustrative numbers, tripling NADH/NAD+ and halving succinate/fumarate widen the span between NAD and Q from 306 mV to 330 mV, raising the free energy per electron pair from −59.0 to −63.8 kJ/mol; at the same time, lower free ADP and inorganic phosphate change the free energy of ATP hydrolysis from −58.1 to −60.9 kJ/mol. The last two lines of the program give two useful rules of thumb: each tenfold change in NADH/NAD+ moves the potential by about 31 mV, and each tenfold change in the product of ADP and phosphate moves the free energy of ATP hydrolysis by about 5.9 kJ/mol.
The calculation shows the internal logic of Veech’s argument: any advantage of ketones lies not in more ATP per molecule of oxygen (they yield less), but in changing the redox state of the couples and the free energy of ATP hydrolysis. It also shows how sensitive the argument is to concentration ratios: changes of a few fold produce differences of tens of millivolts, and these ratios are hard to measure accurately in living tissue.
Where the evidence is, and where it ends
Evidence
The perfused rat heart. In the isolated working heart, Sato and colleagues found that adding ketones (or insulin) to glucose increased hydraulic work without a corresponding increase in oxygen consumption, that is, cardiac efficiency rose; the NAD couple was measured as more reduced, the Q couple more oxidised, and the free energy of ATP hydrolysis larger (Sato et al. 1995). This is the most direct experimental basis of Veech’s hypothesis.
Evidence
The human heart. Nielsen and colleagues infused BHB intravenously into patients with chronic heart failure and found a clear rise in cardiac output without a fall in myocardial external efficiency (Nielsen et al. 2019). How much of the effect came from improved myocardial energy transduction and how much from peripheral vasodilation and lower afterload remains under discussion; nor does it show that oral ketones or a ketogenic diet have the same effect in healthy people.
Evidence
Exercise performance. Cox and colleagues found that trained cyclists who drank a ketone ester along with carbohydrate rode slightly farther in a 30-minute time trial (Cox et al. 2016); Leckey and colleagues found that in professional cyclists a ketone diester made time-trial performance worse, with gastrointestinal discomfort (Leckey et al. 2017). Overall, the effects of exogenous ketones on performance are inconsistent and depend on formulation, dose, type of exercise and whether carbohydrate is taken too. This book gives no dose for any ketone ester or ketone salt product.
The present state of Veech’s hypothesis, then, is this: it has an experimental basis in the isolated heart and its internal logic is consistent; but it relies on concentration ratios that are hard to measure in vivo, and the evidence in the human brain and in exercise performance is inconsistent. “Ketones are a superfuel” goes far beyond the evidence.
Hypothesis · not established
A testable implication of the redox-span hypothesis in humans (not yet established). If ketones really raise myocardial work efficiency by widening the mitochondrial redox span, then in healthy people, raising blood BHB to about 1–2 mmol/L (by fasting or intravenous infusion in a study, not as a dietary recommendation) with cardiac load and peripheral vascular resistance held constant should raise myocardial external efficiency measured by positron emission tomography. If efficiency does not change once load is strictly controlled, the hypothesis is weakened in humans.
Summary
Veech’s thermodynamic argument does not claim that ketones yield more ATP per molecule of oxygen; it claims that ketones change the redox state of mitochondrial couples and the free energy of ATP hydrolysis. The Nernst equation shows that the argument is logically sound but highly sensitive to concentration ratios. Evidence from the isolated heart supports it; evidence from the human heart points the same way but leaves the mechanism unsettled; evidence on exercise performance conflicts. The next chapter turns to another identity of ketones: as signalling molecules.
References
Fan, Y. (2026). Ketone Metabolism, β-Hydroxybutyrate Signalling and the Bioenergetics of Intermittent Fasting: From the Randle Cycle and Epigenetic Inhibition to Autophagy Kinetics, Read Beside Classical Chinese Fasting Texts [酮体代谢、β-羟丁酸信号转导与间歇性禁食的生物能量学] (Version 1.0.0). 5D Library. https://doi.org/10.5281/zenodo.23753263 · Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0).