^ Jump up to: a b c Harris, L; Hamilton, S; Azevedo, LB; Olajide, J; De Brún, C; Waller, G; Whittaker, V; Sharp, T; Lean, M; Hankey, C; Ells, L (February 2018). "Intermittent fasting interventions for treatment of overweight and obesity in adults: a systematic review and meta-analysis". JBI Database of Systematic Reviews and Implementation Reports. 16 (2): 507–547. doi:10.11124/JBISRIR-2016-003248. PMID 29419624.
I started IT about 6 weeks ago. I eat between 12 noon and 8 pm. This works best for me and I have found easily sustainable. The results so far have blown my mind. I have an autoimmune disease and struggled with bloating, multiple food intolerance, gut pain, frequent urination, sugar cravings. All of these symptoms are gone. My hunger is controlled and I can enjoy lovely family dinners again. I think ideally eating earlier in the day would be better, but due to my schedule this works better for me and I am happy with the results.

It is possible to combine the results of several small studies to produce evidence that is stronger than that available from each study alone—a statistical method known as meta-analysis. One of four such analyses, conducted in 2006, looked at 19 studies on a total of 1,084 patients.[23] It concluded that a third achieved an excellent reduction in seizure frequency and half the patients achieved a good reduction.[18]
This is a new area, but the research that has come out since this article is also positive, and promising. One example: In this June 2018 study of 23 people with obesity, 12 weeks of 8-hour time-restricted feeding resulted a 2.6% decrease in body weight and a 7 point decrease in systolic blood pressure, which was significant when compared to controls: https://www.ncbi.nlm.nih.gov/pubmed/29951594
Nuts and seeds make great snacks that are high-fat and can be eaten around 2:30 p.m. Soaking these beforehand can help neutralize naturally occurring enzymes like phytates that can contribute to digestive problems. Eat dinner around 5:30 p.m., and just like the 8-to-6 window plan, a dinner with some sort of wild-caught fish or other clean protein source with vegetables is a great option.
During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt, Jr. and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.[10]
The ketogenic diet is usually initiated in combination with the patient's existing anticonvulsant regimen, though patients may be weaned off anticonvulsants if the diet is successful. Some evidence of synergistic benefits is seen when the diet is combined with the vagus nerve stimulator or with the drug zonisamide, and that the diet may be less successful in children receiving phenobarbital.[18]

Around this time, Bernarr Macfadden, an American exponent of physical culture, popularised the use of fasting to restore health. His disciple, the osteopathic physician Dr. Hugh William Conklin of Battle Creek, Michigan, began to treat his epilepsy patients by recommending fasting. Conklin conjectured that epileptic seizures were caused when a toxin, secreted from the Peyer's patches in the intestines, was discharged into the bloodstream. He recommended a fast lasting 18 to 25 days to allow this toxin to dissipate. Conklin probably treated hundreds of epilepsy patients with his "water diet" and boasted of a 90% cure rate in children, falling to 50% in adults. Later analysis of Conklin's case records showed 20% of his patients achieved freedom from seizures and 50% had some improvement.[10]
Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures, and kidney stones.[18] The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone.[38] About one in 20 children on the ketogenic diet develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramate, zonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone.[39] The stones are treatable and do not justify discontinuation of the diet.[39] Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in one-seventh of the incidence of kidney stones.[40] However, this empiric usage has not been tested in a prospective controlled trial.[9] Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:[39]
In addition, the healthy habits and kinds of foods recommended on the Mayo Clinic Diet — including lots of vegetables, fruits, whole grains, nuts, beans, fish and healthy fats — can further reduce your risk of certain health conditions. The Mayo Clinic Diet is meant to be positive, practical, sustainable and enjoyable, so you can enjoy a happier, healthier life over the long term.
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