Most people, including me, began a ketogenic (low-carb, high-fat) diet to manage my weight. However, there are many other benefits. According to Volek, et al (See peer review evidence) there are other benefits of a ketogenic diet including;
STRONG EVIDENCE TO SUPPORT
- Weight loss
- Cardiovascular disease
- Type 2 diabetes
EMERGING EVIDENCE TO SUPPORT
- Polycystic ovary syndrome
- Alzheimer’s disease
- Parkinson’s disease
- Brain trauma
- Amyotrophic lateral sclerosis
“Very-low-carbohydrate diets or ketogenic diets have been in use since the 1920s as a therapy for epilepsy and can, in some cases, completely remove the need for medication. From the 1960s onwards they have become widely known as one of the most common methods for obesity treatment. Recent work over the last decade or so has provided evidence of the therapeutic potential of ketogenic diets in many pathological conditions, such as diabetes, polycystic ovary syndrome, acne, neurological diseases, cancer and the amelioration of respiratory and cardiovascular disease risk factors. The possibility that modifying food intake can be useful for reducing or eliminating pharmaceutical methods of treatment, which are often lifelong with significant side effects, calls for a serious investigation. This review revisits the meaning of physiological ketosis in the light of this evidence and considers possible mechanisms for the therapeutic actions of the ketogenic diet on different diseases. The present review also questions whether there are still some preconceived ideas about ketogenic diets, which may be presenting unnecessary barriers to their use as therapeutic tools in the physician’s hand.”
WHAT IS KETOSIS (where Ketogenic gets its name)?
According to the published paper, “Insulin activates key enzymes in pathways, which store energy derived from carbohydrates, and when there is an absence or scarcity of dietary carbohydrates the resulting reduced insulin level leads to a reduction in lipogenesis and fat accumulation. After a few days of fasting, or of drastically reduced carbohydrate consumption (below 50 g/day), glucose reserves become insufficient both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle (which gave origin to the phrase ‘fat burns in the flame of carbohydrate’) and for the supply of glucose to the central nervous system (CNS).
The CNS cannot use fat as an energy source; hence, it normally utilizes glucose. After 3–4 days without carbohydrate consumption the CNS is ‘forced’ to find alternative energy sources, and as demonstrated by the classic experiments of Cahill and colleagues this alternative energy source is derived from the overproduction of acetyl coenzyme A (CoA). This condition seen in prolonged fasting, type 1 diabetes, and high-fat/low-carbohydrate diets leads to the production of higher-than-normal levels of so-called ketone bodies (KBs), that is, acetoacetate, β-hydroxybutyric acid and acetone—a process called ketogenesis and which occurs principally in the mitochondrial matrix in the liver. The main KB produced in the liver is acetoacetate but the primary circulating ketone is b-hydroxybutyrate although the latter is not, strictly speaking, a KB because the ketone moiety has been reduced to a hydroxyl group. Under normal conditions of adequate dietary carbohydrate, the production of free acetoacetic acid is negligible and it is rapidly metabolized by various tissues, especially the skeletal and heart muscles. In conditions of overproduction of acetoacetic acid, it accumulates above normal levels and part of it is converted to the other two KBs leading to ketonemia and ketonuria (presence of KBs in the blood and urine). The characteristic ‘sweet’ breath odor of ketosis is caused by acetone, which, being a very volatile compound, is eliminated mainly via respiration in the lungs. The pathway that results in the formation of 3-hydroxy-3-methylglutaryl–CoA from acetyl CoA also occurs in the cytosol of hepatic cells where it is used instead for the biosynthesis of cholesterol. Under normal conditions, the concentration of KBs is very low (<0.3 mmol/l) compared with glucose (~4 mmol), and as glucose and KBs have a similar kM for glucose transport to the brain the KBs begin to be utilized as an energy source by the CNS when they reach a concentration of about 4 mmol/l, which is close to the Km for the monocarboxylate transporter.
KBs are then used by tissues as a source of energy through a pathway that leads to the formation from β-hydroxybutyrate of two molecules of acetyl CoA, which are used finally in the Krebs cycle. It is interesting to note that the KBs are able to produce more energy compared with glucose because of the metabolic effects of ketosis—the high chemical potential of 3-β-hydroxybutyrate leads to an increase in the ΔG0 of ATP hydrolysis. A further point to underline is, as shown in Table 1, that glycaemia, even though reduced, remains within physiological levels because of the fact that glucose is formed from two sources: from glucogenic amino acids and from glycerol liberated via lysis from triglycerides. We would like to emphasize that ketosis is a completely physiological mechanism and it was the biochemist Hans Krebs who first referred to physiological ketosis to differentiate it from the pathological ketoacidosis seen in type 1 diabetes. In physiological ketosis (which occurs during very-low-calorie ketogenic diets), ketonemia reaches maximum levels of 7/8 mmol/l (it does not go higher precisely because the CNS efficiently uses these molecules for energy in place of glucose) and with no change in pH, whereas in uncontrolled diabetic ketoacidosis it can exceed 20 mmol/l with a concomitant lowering of blood pH.”