Understanding Ketogenesis: Anabolism and Catabolism
Ketogenesis is a pretty complicated process and can create a lot of confusion. I know a lot of people on Keto diets that would say too much protein could turn into carbs (hint: they probably don’t). I see a lot of others say you can build muscle easier on a ketogenic diet, with the same or less dietary protein(hint: you probably can’t, no matter what Wilson, Lowery, & co. say). The key to understanding ketogenesis and why the aforementioned statements are true lies in understanding catabolic and anabolic reactions.
Catabolism, in brief, is the breakdown of large molecules into smaller ones. In the context of metabolism, these smaller substrates are things such as TCA Cycle intermediates/products or ketones from fat/ketogenic amino acids. Anabolism is the opposite; creating larger things from smaller ones, such as gluconeogenesis or building muscle.
Catabolic/anabolic states in humans are largely regulated by insulin and glucagon.
Insulin is a potent stimulator for anabolism — increasing muscle, storage of fat — but also regulates some catabolic reactions. For example, insulin will promote catabolism of carbohydrates. Overall, however, insulin is anabolic because the overall state of the body switches to storage mode. Even though insulin can increase the rate of glucose metabolism, increased glycolysis directly contributes to lipogenesis and the storage of fatty acids. Extra substrates from glycolysis that aren’t used for energy production are subsequently turned into fatty acids.
Similarly, glucagon stimulates catabolism (i.e. fatty acid metabolism, protein degredation, etc.), but also can regulate some anabolic reactions. Glucagon is a key regulator of gluconeogenesis — thus, even though the body may be in an overall catabolic state by breaking down fatty acids and protein, some anabolic reactions may occur (like gluconeogenesis).
Anabolic reactions (like GNG) in a catabolic state and catabolic reactions (like glycolysis) in an anabolic state are important for proper homeostasis. Glycolysis after feeding and the presence of insulin (anabolic) prevents possible hyperglycemia in the context of high consumption of carbs. GNG during times of fasting (catabolic) prevents hypoglycemia. There is a strict level of homeostasis that the body must maintain for survival.
Understanding these reactions and their physiological conditions are important to understanding how and why ketogenesis works and its importance.
Extra protein in the diet doesn’t cause much GNG because of the insulin response to ingestion of protein, which shuts down GNG and stimulates muscle protein synthesis.
N.B. I say it doesn’t cause much GNG because glucagon is also released during protein ingestion, though the insulin:glucagon ratio is still high enough to prevent most GNG.
Similarly, the lower insulin response from protein relative to carbohydrates and the simultaneous glucagon release make muscle protein synthesis a little bit harder to manage in a low-carb diet. Additionally, insulin is present for longer periods of time following a meal containing high(ish) amounts of carbs, meaning the anabolic state (and muscle protein synthesis) lasts longer on a high-carb diet than on a low-carb diet.
Additionally, the insulin response created by protein ingestion will probably inhibit lipolysis and the production of ketones for a short time, but will return back to fasting levels relatively quick. This is why protein restriction during weight loss on a low-carb diet is not necessary, and may actually be harmful. You should consume a little extra protein to compensate for the loss of protein created during the catabolic state created during low-carb diets. Unless you’re going keto for medical reasons, excess protein can only be beneficial to your progress.
Even excess protein in medical conditions may not be so bad, IMO. But I’ll leave that to future research.
