Table 2.
Probable Anti-Seizure Mechanisms Of KD
| Primary Physiological Change | Probable Hypothesized Mechanism Of Seizure Reduction |
|---|---|
| (a) Ketosis | (i) Hyperpolarization of neurons by Potassium channel activation |
| (ii) Slow energy production (compared to pathway wherein energy is derived primarily from glucose) which leads to anti-seizure effects | |
| (iii) Potentiation of inhibitory neurotransmitters (eg, GABA) | |
| (iv) Augmented neuronal function through cellular | |
| (v) Chronic ketosis is postulated to stabilize and reduce synaptic hyperexcitability in order to conserve energy, thereby increasing seizure threshold | |
| (b) Increased levels of Polyunsaturated Fatty Acids (PUFA) | (i) Activation of e peroxisome proliferator-activated receptors (PPARs) |
| (ii) Hyperpolarization of neurons | |
| (c) Alteration of gut microbiome | Possible role in increasing seizure threshold due to putative microorganisms (eg, Akkermansiamuciniphila and Parabacteroides) which has been noted in murine models as well as human studies of gut microbiome |
| (d) Alteration of proinflammatory and anti-inflammatory mediators | Reduced levels of Interleukin 1b and other proinflammatory cytokines in mice treated with KD supports the role of modulation of these inflammatory mediators in combating epilepsy |