As an additional example, established
anticonvulsant effects of ketogenic diets in humans and rats are countered by only mixed success in mice in various seizure models.54, 55, 56 Therefore, mice might be a challenging model for exploring the relationship between a ketogenic diet and pain and inflammation.
Logically, then, if there is any commonality in the actions
of anticonvulsant drugs and the
ketogenic diet, the latter should have some
effect on neuropathic pain.
For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production
of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation
of synaptic function.80 Moreover, the increased synthesis
of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation
of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability
of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism,
ketogenic diets may activate
anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective
effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition
of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits
of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception
of its use in the treatment
of convulsion diseases.