Because some cancer cells are inefficient in processing ketone bodies for energy, the ketogenic diet has also been suggested as a treatment for cancer.[59][60] A 2018 review looked at the evidence from preclinical and clinical studies of ketogenic diets in cancer therapy. The clinical studies in humans are typically very small, with some providing weak evidence for anti-tumour effect, particularly for glioblastoma, but in other cancers and studies, no anti-tumour effect was seen. Taken together, results from preclinical studies, albeit sometimes contradictory, tend to support an anti-tumor effect rather than a pro-tumor effect of the KD for most solid cancers.[61]


The brain is composed of a network of neurons that transmit signals by propagating nerve impulses. The propagation of this impulse from one neuron to another is typically controlled by neurotransmitters, though there are also electrical pathways between some neurons. Neurotransmitters can inhibit impulse firing (primarily done by γ-aminobutyric acid, or GABA) or they can excite the neuron into firing (primarily done by glutamate). A neuron that releases inhibitory neurotransmitters from its terminals is called an inhibitory neuron, while one that releases excitatory neurotransmitters is an excitatory neuron. When the normal balance between inhibition and excitation is significantly disrupted in all or part of the brain, a seizure can occur. The GABA system is an important target for anticonvulsant drugs, since seizures may be discouraged by increasing GABA synthesis, decreasing its breakdown, or enhancing its effect on neurons.[7]

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]
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]
There were [no statistical] differences between the low- and high- [meal frequency] groups for adiposity indices, appetite measurements or gut peptides (peptide YY and ghrelin) either before or after the intervention. We conclude that increasing meal frequency does not promote greater body weight loss under the conditions described in the present study.
Probably, and there are a few reasons why the keto diet usually equals weight-loss gold, says Keatley. For starters, people usually reduce their daily caloric intake to about 1,500 calories a day because healthy fats and lean proteins make you feel fuller sooner—and for a longer period of time. And then there’s the fact that it takes more energy to process and burn fat and protein than carbs, so you're burning slightly more calories than you did before. Over time, this can lead to weight loss.
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]

The word diet first appeared in English in the 13th century. Its original meaning was the same as in modern English, “habitually taken food and drink.” But diet was used in another sense too in the Middle and early modern English periods to mean “way of living.” This is, in fact, the original meaning of diet’s Greek ancestor diaita, which is derived from the verb diaitasthan, meaning “to lead one’s life.” In Greek, diaita, had already come to be used more specifically for a way of living prescribed by a physician, a diet, or other regimen.
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