When we say ketones, our company is discussing the primary circulating fatty acid metabolites beta-hydroxybutyrate (OHB) and acetoacetate (AcAc). More on ketone basics here. Exogenous ketones (also referred to as ketone supplements) and well-formulated ketogenic diets share a minumum of one thing in common. Both of them result in increased circulating concentrations of beta-hydroxybutyrate (BOHB), but ultimately are related to totally different patterns of ketosis, in addition to differing metabolic and physiologic outcomes. In short, they should not be assumed to have equivalent effects since they achieve similar BOHB blood levels. With that said, there are many reasons we need to continue to study the various forms and potential uses of keto mineral supplements.
Within the last few million years, the only method for humans to utilize ketones for fuel would be to restrict carbohydrates low enough and for long enough to induce the liver to ensure they are. This really is admittedly hard for many people to accomplish in a world that still believes that dietary carbs are good and fats are bad. An emerging alternative is always to consume ketones being a dietary supplement. The study into how these function within the body and what benefits they can confer remains early stage, but we already have numerous such products available for sale. In this particular section, we shall discuss how exogenous ketones affect blood ketone levels, and exactly how they may influence health insurance and disease compared to ketones produced within your body.
The two predominant ketones produced by the liver are beta-hydroxybutyrate (BOHB) and acetoacetate (AcAc). Here’s a brief summary of basic information regarding these ketones:
It is estimated that the keto-adapted adult can make 150 or maybe more grams of ketones daily after adapting to an overall total fast (Fery 1985), and perhaps 50-100 grams daily on the well-formulated ketogenic diet.
Some AcAc naturally stops working to form acetone, which comes out with the lungs and kidneys, giving a chemical odor for the breath when ketones are high.
A lot of the AcAc manufactured in the liver is acquired by muscle and transformed into BOHB.
Within the keto-adaptation process, how muscles and kidneys cope with BOHB and AcAc changes over the first few weeks and months, and so the ratio of AcAc to BOHB inside the blood changes considerably in the first couple of weeks.
Whilst the ultimate fate of most ketones in the blood is going to be burned for fuel, BOHB and AcAc appear to have differing roles in regulating genes and cellular functions.
Particularly with gene regulation, BOHB appears to play a more significant regulatory role than AcAc, but AcAc could have a particular role in signaling muscle regeneration .
Sources and Formulations of Exogenous Ketones – The 2 compounds commonly referred to as ‘ketone bodies’ (BOHB and AcAc) are designed and used for multiple purposes across nature from algae to mammals, but seldom in concentrations useful for extraction as human food. Because of this, the cause of the majority of exogenous ketones is chemical synthesis. Furthermore, most current research and utilize of ketone supplements targets BOHB. That is because AcAc is chemically unstable – it slowly stops working to create acetone by releasing loejbp one molecule of CO2.
In a keto-adapted individual where ketone metabolism is brisk with up to 100 grams or more being oxidized (i.e., ‘burned for energy’) daily, the tiny amount lost in breath and urine as acetone is minor. But as this breakdown occurs spontaneously without the need for the help of enzymes, in addition, it occurs to AcAc in a stored beverage or food (even in an air-tight container), making the shelf-life of AcAc-containing products problematic. Thus all current ketone supplements include BOHB in certain form rather than the natural mix of BOHB and AcAc produced by the liver.
Another significant distinction between endogenous and exogenous BOHB is that most synthetic BOHB used in health supplements is a combination of both ‘D’ and ‘L’ isomers, whereas endogenously produced BOHB includes only the D-isomer. Metabolically, the 2 isomers are very different, and current published information shows that a lot of the energy and signaling advantages of BOHB derive through the D-form. This can be potentially problematic since the L-isomers are certainly not metabolized through the same chemical pathways since the D-forms (Lincoln 1987, Stubbs 2017), plus it remains unclear whether humans can convert the L-form to the D-form.
Thus, while the L-isomers tend not to seem to be toxic, they are not very likely to impart exactly the same benefits as the D-forms. Additionally, the existing assays for blood ketones are specific towards the D-isomer, so it is difficult to track blood levels and clearance for any L-isomer taken in a supplement.