Is Dietary Ketosis Harmful To The Liver?
The mild dietary ketosis, such as that which is experienced during the Weight Loss phase of the Lean for Life program, is not harmful to individuals with a normal, healthy, functioning liver. Here is some information about ketosis that may help you to understand its role in weight loss: The carbohydrates you eat are converted to glucose, which is the body’s primary source of energy. Whenever your intake of carbohydrates is limited to a certain range, for a long enough period of time, you’ll reach a point where your body draws on its alternate energy system, fat stores, for fuel. This means your body burns fat and turns it into a source of fuel called ketones. (Ketones are produced whenever body fat is burned.) When you burn a larger amount of fat than is immediately needed for energy, the excess ketones are discarded in the urine. Being in ketosis means your body has burned a large amount of fat in response to the fact that it didn’t have sufficient glucose available for energy needs. Dietary ketosis is among the most misunderstood concepts in nutrition because it is often confused with ketoacidosis, which is a life-threatening condition most often associated with uncontrolled insulin-deficient Type 1 diabetes. In the Type 1 diabetic, the absence of insulin leads to a toxic build-up of blood glucose and an extreme break-down of fat and muscle tissue. This condition doesn’t occur in individuals who have even a small amount of insulin, whether from natural production or artificially administered. Dietary ketosis, however, is a natural adjustment to the body’s reduced intake of carbohydrates as the body shifts its primary source of energy from carbohydrates to stored fat. The presence of insulin keeps ketone production in check so that a mild, beneficial ketosis Continue reading >>
How Does Keto//os Affect Kidneys And Liver And The Role In Metabolizing Ketones?
As with all medium chain triglycerides, the MCT powder portion of the product will largely be converted to ketones by the liver within a few short hours of consumption. MCT create a readily supply of Ketone production for the liver to use for ketones. The BHB-salt portion should simply be absorbed into the blood as ketones. The BHB supplies another source, which doesn’t require the liver to produce ketones. There is no reason that the ketones produced by the product will affect the kidneys or liver any differently than ketones produced from exogenous fats (such as when eating a ketogenic diet) or ketones produced from stored fats (such as when calorie restricting or losing weight). Exogenous ketone scientific literature does not suggest that either kidney or liver function is negatively affected by ketosis. The major role of the kidneys when it comes to ketones is to excrete excess ketones in the urine. This excretion will likely be highest during the first few days of keto-adaptation (either in eating the keto diet or consuming KETO//OS), but the body will retain more and the tissues will begin to preferentially burn the ketones as consumption continues. The liver is the major site of endogenous ketone production, so taking exogenous ketones with KETO//OS would provide another source besides the liver to make ketones. Remember, KETO//OS and exogenous ketones are a source of calories; so be sure to consider it in your daily goals. KETO//OS and exogenous ketone supplementation is not hard on the liver. Continue reading >>
Ketosis And Fatty Liver
Fatty liver is usually associated with alcohol abuse, but even people who don't drink can develop nonalcoholic fatty liver disease, or NAFLD. NAFLD includes asymptomatic steatosis, meaning simple fatty liver, which can progress to steatohepatitis, meaning inflamed fatty liver. Later, the disease can cause fibrosis, or scarring, and ultimately cirrhosis, which is permanent. Alcoholic fatty liver can only be treated by abstaining from alcohol in the early stages of the disease. But, because NAFLD is likely diet-related, it might be reversible by substantially reducing carbohydrate intake by means of a ketogenic diet. Video of the Day NAFLD is associated with obesity -- especially abdominal, insulin resistance, elevated blood sugar, inflammation and high serum triglycerides. These are all signs of metabolic syndrome, considered the precurser to Type 2 diabetes. When the body cannot use sugar properly, some of it is converted to fat -- triglycerides -- by the liver, where it can accumulate. A 2009 study conducted at the Center for Human Nutrition and Atkins Center of Excellence in Obesity Medicine found that excess liver fat is probably the major culprit behind the health issues often associated with obesity. The Ketogenic Diet The ketogenic diet is a high-protein, high-fat, carbohydrate-restricted diet usually used for weight loss. Reducing or eliminating dietary carbohydrate forces the body to rely on stored fat for energy. However, the body metabolizes fat differently in the absence of carbohydrates, resulting in a condition called ketosis. Incompletely metabolized fat forms molecules called ketones, which accumulate in the blood and urine. Ketones have limited value as an energy source in the absence of carbohydrate, mainly for the brain, but most are excreted in the ur Continue reading >>
Conditions Leading To Liver Damage
Symptoms that are indicative of reduced liver function or possible liver damage include general malaise, fatigue, digestive disturbances (eg, constipation), allergies and chemical sensitivities, weight loss, jaundice, edema, and mental confusion. Generalized pruritus (itching), nausea, and vomiting can also result from impaired liver function. Causes of liver damage are numerous and may include congenital defects (malformed or absent bile ducts), obstructed bile ducts (cholestasis), autoimmune disorders, metabolic disorders (hemochromatosis, Wilson's disease), tumors, toxins (drugs, overdoses, poisons), alcohol-related conditions (cirrhosis), bacterial and parasitic infections, and viral infections (hepatitis B and C). This section discusses several chronic disorders and diseases that can lead to degenerative liver damage without proper diagnosis and treatment. Cholestasis Cholestasis is interruption or stagnation of bile flow in any part of the biliary system, beginning with the liver. Cholestasis has several causes, including obstruction of the bile ducts by the presence of gallstones or a tumor, drug and alcohol use, hepatitis, and existing liver disease (Glanze 1996). In the United States, an important cause of cholestasis and impaired liver function is the consumption of alcohol. Other common causes of cholestasis are viral hepatitis and drugs, particularly steroidal hormones (including estrogen and oral contraceptives). Cholestasis can cause alterations of liver function tests, indicating cellular damage. In the initial stages of liver dysfunction, standard tests (serum bilirubin, alkaline phosphatase, SGOT, LDH, GGTP, etc.) may not be sensitive enough to be of value for complete, early diagnosis. However, measurement of serum bile acids is a safe, sensitive test Continue reading >>
Effects Of Liver Damage On Ketone-body Production And Nitrogen Balance In Starved Rats.
Abstract The metabolic effects of intraperitoneal administration of carbon tetrachloride (1ml/kg) were studied in starved rats. The most notable change in circulating substrates was an 80% fall in ketone-body concentrations, which was associated with the doubling of urinary nitrogen losses. The results demonstrate the importance of starvation ketosis in permitting fat mobilization to decrease effectively protein losses during starvation. Continue reading >>
Ketone Bodies
Ketone bodies Acetone Acetoacetic acid (R)-beta-Hydroxybutyric acid Ketone bodies are three water-soluble molecules (acetoacetate, beta-hydroxybutyrate, and their spontaneous breakdown product, acetone) that are produced by the liver from fatty acids[1] during periods of low food intake (fasting), carbohydrate restrictive diets, starvation, prolonged intense exercise,[2], alcoholism or in untreated (or inadequately treated) type 1 diabetes mellitus. These ketone bodies are readily picked up by the extra-hepatic tissues, and converted into acetyl-CoA which then enters the citric acid cycle and is oxidized in the mitochondria for energy.[3] In the brain, ketone bodies are also used to make acetyl-CoA into long-chain fatty acids. Ketone bodies are produced by the liver under the circumstances listed above (i.e. fasting, starving, low carbohydrate diets, prolonged exercise and untreated type 1 diabetes mellitus) as a result of intense gluconeogenesis, which is the production of glucose from non-carbohydrate sources (not including fatty acids).[1] They are therefore always released into the blood by the liver together with newly produced glucose, after the liver glycogen stores have been depleted (these glycogen stores are depleted after only 24 hours of fasting)[1]. When two acetyl-CoA molecules lose their -CoAs, (or Co-enzyme A groups) they can form a (covalent) dimer called acetoacetate. Beta-hydroxybutyrate is a reduced form of acetoacetate, in which the ketone group is converted into an alcohol (or hydroxyl) group (see illustration on the right). Both are 4-carbon molecules, that can readily be converted back into acetyl-CoA by most tissues of the body, with the notable exception of the liver. Acetone is the decarboxylated form of acetoacetate which cannot be converted Continue reading >>
Effects Of Liver Damage On Ketone-body Production And Nitrogen Balance In Starved Rats
The metabolic effects of intraperitoneal administration of carbon tetrachloride (1ml/kg) were studied in starved rats. The most notable change in circulating substrates was an 80% fall in ketone-body concentrations, which was associated with the doubling of urinary nitrogen losses. The results demonstrate the importance of starvation ketosis in permitting fat mobilization to decrease effectively protein losses during starvation. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (444K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References. These references are in PubMed. This may not be the complete list of references from this article. Continue reading >>
