Gluconeogenesis

Isn’t that a fun word? I don’t know why I seem to enjoy it so much, but just about anything with the suffix “-genesis” gets me riled up. Gluconeogenesis. Ketogenesis. Phil Collins’ Genesis. Well, maybe not so much Phil Collins.

Can you smell the ketones in your breath tonight?

Anyway, gluconeogenesis (GNG) is talked about a lot in the dieting world, more specifically in the ketosphere. The story goes something like this: Your body can only handle X amount of protein at at time, so excess protein is broken down and later used for gluconeogenesis.” To take things further, words of a [not-so] wise charlatan in the ketosphere alluded excess protein, like steak, to the equivalent of eating chocolate cake.

That’s bullshit. Study: Protein doesn’t really do much to increase blood glucose. In this study, 50 grams of protein was only estimated to account for about 4 grams of glucose in the blood. That’s 8%. And that was after a 12 hour fast. The authors concluded that whatever protein wasn’t used by the body was excreted in the urine. So basically, use it or lose it.

Note: There have been other studies that suggest that infusion of protein induces GNG, which is probably where this rumor came about; however, things seem to be a little different when the protein is ingested rather than added directly to the blood.

Now, could more than 50 grams of protein induce more GNG? Maybe. There could also be a ceiling effect, too. I don’t know of any data to sway the argument either way, so for now I’m going to take the study as the best data we have and assume protein doesn’t do much to influence glucose levels.

No matter what the reasoning is, this fear of gluconeogenesis usually stems around inhibition of ketogenesis. I think it’s silly and unfounded unless you’re trying to induce medical ketosis, but more on that for a later blog post.

The simple fact is that food is an inhibitor of ketogenesis. All food. There are no exceptions to this rule.

In order to induce ketogenesis there has to be a good degree of lipolysis and fatty acid breakdown to produce enough Acetyl CoA and create ketone bodies. There are many regulating hormones involved in inducing the metabolism of fats: epinephrine and norepinephrine released during exercise, for example, are known to increase fatty acid metabolism and be a major contributing factor to post-exercise ketosis (also known as the Courtice-Douglass Effect).

The major hormones involved in fatty acid metabolism in resting states that are impacted by diet are none other than glucagon and insulin. In short, glucagon stimulates release and breakdown of fats and glycogen while insulin promotes the storage and synthesis of fats and glycogen. When glucagon is high (like during fasting or states where glucose is low-ish), breakdown of fats and glycogen begin. In the ketoadapted state, it appears that the body is more inclined to spare glycogen and favor breakdown of fat, inducing a state of ketosis (in non-adapted states, it seems glycogen is broken down with a little more preference than fats). When insulin is high, fat breakdown comes to a near halt (it doesn’t make sense to be breaking down a lot of fat while also trying to store it, does it?)

Here’s the thing: nearly every food you eat stimulates insulin release.

Holt, Miller, & Petocz, 1997

That steak we talked about early probably induces a higher magnitude of insulin release than the chocolate cake, albeit at a shorter duration than the cake, and I would bet dietary fat has a similar response.

Nuttall & Cannon, 2004

All of this makes sense because we already know that fasting is the most efficient and most potent method of inducing ketosis, because of high levels of glucagon and low levels of insulin. Food causes these mechanisms to disontinue. Which is the reason why this guy had low ketones after eating a meal.

So please, don’t attribute falling out of ketosis to protein. And for the love of humanity, don’t compare steak to cake.

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