Table 1.
Disorder | Highest clinical class of evidence | Potential mechanisms of action |
---|---|---|
Neurologic | ||
Epilepsy | I | Enhanced mitochondrial function, fatty acid effect on ion channels, neurotransmission and neurotransmitters, decreased effects from reactive oxygen species |
Alzheimer disease/cognitive impairment | I | Decreased beta amyloid deposition, relief of block in PDH |
Parkinson’s disease | III | Enhanced mitochondrial function |
Amyotrophic lateral sclerosis | Enhanced mitochondrial function | |
Traumatic brain injury | Substrate delivery, enhanced mitochondrial function | |
Hypoxic/ischemic brain injury | Substrate delivery, enhanced mitochondrial function | |
Autism | III | Enhanced mitochondrial function |
Depression | III | Enhanced mitochondrial function |
Headaches | III | Enhanced mitochondrial function |
Narcolepsy | III | Enhanced mitochondrial function |
Metabolic | ||
GLUT-1 deficiency | III | Substrate delivery |
PDH deficiency | III | Substrate delivery |
PFK deficiency | III | Substrate delivery |
Glycogenosis type V (McArdle disease) | III | Substrate delivery |
Other | ||
Cancer (astrocytomas, prostate, gastric) | III | Substrate delivery |
Cardiac ischemia | Substrate delivery, enhanced mitochondrial function |
GLUT-1—glucose transporter type 1; PDH—pyruvate dehydrogenase; PFK—phosphofructokinase.