This article is more suggestive than anything, but I believe some on this board have reported improvement on the Atkins diet or other diets regulating blood glucose levels. I have been experimenting with intermittent fasting with some success.
The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders
Carl E. Stafstrom and Jong M. Rho
Frontiers in Pharmacology 2012; 3: 59.
Dietary and metabolic therapies have been attempted in a wide variety of neurological diseases, including epilepsy, headache, neurotrauma, Alzheimer disease, Parkinson disease, sleep disorders, brain cancer, autism, pain, and multiple sclerosis. The impetus for using various diets to treat – or at least ameliorate symptoms of – these disorders stems from both a lack of effectiveness of pharmacological therapies, and also the intrinsic appeal of implementing a more “natural” treatment. The enormous spectrum of pathophysiological mechanisms underlying the aforementioned diseases would suggest a degree of complexity that cannot be impacted universally by any single dietary treatment. Yet, it is conceivable that alterations in certain dietary constituents could affect the course and impact the outcome of these brain disorders. Further, it is possible that a final common neurometabolic pathway might be influenced by a variety of dietary interventions. The most notable example of a dietary treatment with proven efficacy against a neurological condition is the high-fat, low-carbohydrate ketogenic diet (KD) used in patients with medically intractable epilepsy. While the mechanisms through which the KD works remain unclear, there is now compelling evidence that its efficacy is likely related to the normalization of aberrant energy metabolism. The concept that many neurological conditions are linked pathophysiologically to energy dysregulation could well provide a common research and experimental therapeutics platform, from which the course of several neurological diseases could be favorably influenced by dietary means. Here we provide an overview of studies using the KD in a wide panoply of neurologic disorders in which neuroprotection is an essential component.
The full article and PDF are available from The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders
Here’s the section on Migraine.
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The KD in Migraine
Migraine is a paroxysmal neurological disorder having considerable clinical phenotypic overlap with epilepsy (Rogawski, 2008). Although the intrinsic mechanisms underlying seizures and migraine attacks differ in many fundamental respects, there are theoretical reasons to consider the KD for chronic migraine. Both disorders involve paroxysmal excitability changes in the brain, and there is considerable overlap in the array of pharmacological agents used to treat these conditions. Although it might seem unlikely that an individual with migraine would undertake such a complicated dietary regimen as the KD, in light of suboptimal alternatives, this choice is worthy of consideration, particularly in the medically refractory population (Maggioni et al., 2011).
Interestingly, the first report of using the KD for migraine came in 1928, only a few years after the diet’s first use for epilepsy (Schnabel, 1928). Nine of 28 patients reported “some improvement,” although the validity of this clinical study is uncertain and some patients admitted poor compliance. Compliance might be better with the less restrictive modified Atkins diet, which has also shown promise for migraine treatment (Kossoff et al., 2010). Other case reports exist but there are no large clinical series or trials. Notwithstanding this limitation, laboratory investigations have found that both short-term and long-term treatment with either MCT or long-chain triglyceride forms of the KD resulted in a significant reduction in the velocity of cortical spreading depression (CSD) velocity in immature rats (de Almeida Rabello Oliveira et al., 2008). Another intriguing aspect of this study was the observation that triheptanoin – an anaplerotic substrate that enhances tricarboxylic acid cycle function – had a notable effect in retarding CSD, consistent with a later report that triheptanoin supplementation raised pentylenetetrazol tonic seizure threshold and delayed the development of corneal kindled seizures (Willis et al., 2010).
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