The trick with the rice is to find a substitute, and we’ve already looked at cauliflower rice. Avoid over grating your cauliflower. You don’t want it so fine that it is a fine powder for this dish. It still needs to have a rice texture. You will also need to add some cream cheese to the cauliflower to work for this rice substitute. Otherwise you’ll just get the cauliflower everywhere!
One hypothesised contributor to neuronal death is insufficient energy production, secondary to impaired mitochondrial function. However, it is unclear if this is in fact a cause or effect of PD. Whatever the case may be, patients with PD have been shown to have impaired mitochondrial energy production in the brain59 and lower brain glucose utilisation60. Another factor may be neuro-inflammation, which is also common in PD, and is thought to lead to further accumulation of Lewy Bodies and neuronal death.
Because the ketogenic diet alters the body's metabolism, it is a first-line therapy in children with certain congenital metabolic diseases such as pyruvate dehydrogenase (E1) deficiency and glucose transporter 1 deficiency syndrome, which prevent the body from using carbohydrates as fuel, leading to a dependency on ketone bodies. The ketogenic diet is beneficial in treating the seizures and some other symptoms in these diseases and is an absolute indication. On the other hand, it is absolutely contraindicated in the treatment of other diseases such as pyruvate carboxylase deficiency, porphyria and other rare genetic disorders of fat metabolism. A person with a disorder of fatty acid oxidation is unable to metabolise fatty acids, which replace carbohydrates as the major energy source on the diet. On the ketogenic diet, their body would consume its own protein stores for fuel, leading to ketoacidosis, and eventually coma and death.
Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures and kidney stones. 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. About 1 in 20 children on the ketogenic diet will 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. The stones are treatable and do not justify discontinuation of the diet. Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in a sevenfold decrease in the incidence of kidney stones. However, this empiric usage has not been tested in a prospective controlled trial. Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:
Beta-hydroxybutyrate (BHB) – Not technically a ketone but a molecule. Its essential role in the ketogenic diet makes it count as the important ketone body. BHB is synthesized by your liver from acetoacetate. BHB is important because it can freely float throughout your body in your blood, crossing many tissues where other molecules can’t. It enters the mitochondria and gets turned into ATP (adenosine triphosphate), the energy currency of your cells. BHB = ATP = energy!