With all the focus on the weight loss effect of a low carb high fat / ketogenic diet, while appropriate because the weight loss is indeed often dramatic, many other potential benefits are often overlooked. In April 2012 an article “The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders” was published that nicely summarizes what’s currently know about the effects a ketogenic diet has on multiple neurological problems. Here is a summary of this paper:
Your brain digs keto.
A ketogenic diet can help with a lot of neurological problems. It does not work for everything, but it clearly seems to be good for you in the long term.
KD works very well. That is now no more doubt about that.
With the KD, rates of degeneration of certain neural structures and functions might be slowed. KD is likely to involve other neuroprotective mechanisms that could ameliorate pathological aging.
Clinical studies to date have been equivocal but promising. Recent studies have shown a closer linkage of AD to epilepsy. there is growing evidence that the KD may be an effective treatment for AD through a variety of metabolism-induced mechanisms that reduce oxidative stress and neuroinflammation, and enhance bioenergetic profiles – largely through enhanced mitochondrial functioning
A small clinical study demonstrated that 5 of 7 affected patients showed improved scores on a standard PD rating scale. However, a placebo effect cannot be ruled out.
Amyotrophic Lateral Sclerosis
Administration of a KD to mice led to both histological (higher motor neuron counts) and functional improvements. However, the KD did not extend survival time.
Theoretically, depriving rapidly dividing, highly metabolic cancer cells of their usual fuel supply, e.g., glucose, could be clinically therapeutic. Animals with experimentally produced brain tumors placed on a KD exhibit markedly decreased tumor growth rates, and these remarkable effects appear to be a consequence of calorie restriction (i.e., reduced blood glucose levels) rather than KD-induced ketosis (i.e., fatty acid oxidation) as the principal mechanism. A pilot trial of the KD in 16 patients with advanced metastatic tumors, six individuals reported improved emotional functioning and less insomnia. It may be that distinct tumor types within different organ systems may respond differently to the KD or other dietary treatments.
To date, no clinical trials of the KD have been performed in patients with stroke, but several animal studies of hypoxia-ischemia support the potential beneficial effect of the diet.
KD was both safe and effective in 14 pediatric patients with established mitochondrial defects in complexes I, II, and IV, all of whom had medically intractable epilepsy. However, KD treatment is not recommended in individuals with primary carnitine deficiencies and fatty acid ß-oxidation abnormalities.
Pre-treatment with a KD significantly reduced cortical contusion volume in an age-related manner that correlated with maturation-dependent differences in cerebral metabolism and ketone utilization. With respect to anti-epileptogenesis following head injury, the data regarding KD effects are mixed.
In rats, KD led to a beneficial effect similar to that afforded by conventional antidepressants. No clinical studies have been conducted.
10 of 18 autistic children demonstrated moderate or significant behavioral improvement (by a blinded rater) after a 6-month trial.
In 1928, 9 of 28 patients reported “some improvement,” although the validity of this clinical study is uncertain and some patients admitted poor compliance. laboratory investigations have found that KD treatment resulted in a significant reduction in the velocity of cortical spreading depression (CSD) velocity in immature rats.