Starting way back in 1931 (when Otto Warburg was awarded his Nobel Prize for research on the link between cancer and adequate oxygen to the cells), there has been a growing body of evidence indicating the link between immune deficiency and
reduced oxygen metabolism.
Not exact matches
HIF - 1 senses
reduced oxygen levels and triggers many changes in cellular function, including a changed
metabolism and sending signals for the formation of new blood vessels.
One possibility, advanced by the Wisconsin team, is that restricting food consumption
reduces the production of tissue - damaging
oxygen free radicals that are a byproduct of food
metabolism.
Also, in both cell culture and a mouse model of the condition, blocking the excessive splintering
reduced production of reactive
oxygen species, a potentially harmful byproduct of
metabolism, as well as cell death.
Used in ancient times to alleviate cramp like symptoms, promote smooth functioning of the endocrine glands, protect joints from wear and tear, alleviate arthritic and rheumatic diseases, and also assists with improving blood circulation, energy, detoxification,
reducing inflammation, stabilizing
metabolism and improving
oxygen use.
Reduce the harmful byproducts of carbohydrate
metabolism called Reactive
oxygen species (ROS).
By restoring the body's natural electro - magnetic energy through PEMF therapy, cell
metabolism is boosted, blood cells are regenerated, circulation is improved,
oxygen carrying capacity is increased and inflammation is
reduced.
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.