However, with the ketone esters, the effects are nearly immediate, and my entire body was humming throughout the entire day, but not in a jittery way. I was full of mental and physical energy that lasted without any sort of crash (it was a gradual taper). During my cognitive tests, things felt almost effortless as I played the various games. After my experiment was complete I continued writing code for several hours, then went to the gym to work out. I did forget to each lunch though, so there must be some suppressive effect on appetite.
In addition, the body regulates ketone production via ketonuria (peeing out excess ketones) and ketone-induced insulin release, which shuts off hepatic ketogenesis (the liver making more ketones when you have enough).   The insulin from this process could be increasing glucose disposal which, when coupled with PDH activation, could drive glucose levels quite low.

Hi- Thank you for this super helpful post. I’m new to Keto and supplementing Keytones. I just got the Julian Bakery Keytones and am curious about how to take them as there are no instructions on the packaging. Indeed the website has a diet plan to follow with the keytones but I am very suspicious of it because it is 0 fat which I believe is not healthy for brain or body and given that I have soft tissue and joint issues, I try to eat enough fat daily. I want to lose weight and I crossfit 5 days per week. So how do I best start with using the keytone supplements? I took a scoop full yesterday when they arrived (in the early afternoon) but hadn’t yet eaten and I think that was a mistake because I had immediate diarrhea which lasted a few hours, even after eating.
Will taking exogenous slow down my fat loss? Since now before digging into my body for energy/ketones, I will first use up the exogenous ketones I ingest. Also do exogenous ketones somehow help get even more keto adapted, keeping in mind I have been on a strict keto diet without a problem and don’t mind it at all. Outside of performance improvements, do you think exogenous ketones is for someone like me who is primarily looking for fat loss.
Exogenous ketones drinks are growing in popularity as a method to elevate blood ketone concentrations and mimic a ketogenic diet without the need for dietary changes (Ari et al., 2016; Cox et al., 2016; Kesl et al., 2016; Caminhotto et al., 2017; Evans et al., 2017). The present study describes the pharmacokinetic and pharmacodynamics properties of ketone ester and salt drinks in humans at rest, and characterizes the effects of a prior meal, which is pertinent to use as a dietary supplement. The main findings were that KE drinks elevated blood d-βHB > 50% higher than KS drinks, the latter significantly increasing blood l-βHB, which was metabolized more slowly by the body. Both drinks had similar effects on FFA, TG, glucose and electrolyte concentrations, although with disparate effects on pH. A prior meal decreased total blood d-βHB appearance after a KE drink. Finally, either three KE drinks or nasogastric feeding effectively maintained nutritional ketosis over 1 mM for 9 h.
Of course, there may be some people who choose to take these supplements because they genuinely do feel they benefit from them. This is of course your choice and this article in no way aims to shame or criticize anybody. However, I do think that, for most people, eating a low-carb diet based on real foods is a lot more likely to be associated with the benefits that the supplements claim to provide than the supplements themselves.
KE consumption decreased FFA from 0.6 to 0.2 mM, TG from 1.0 to 0.8 mM, and glucose from 5.5 to 4.7 mM by the end of the study (4 h). The effect was not altered by a meal (Figures 5A–C). Dextrose drinks also lowered FFA from 0.6 to 0.2 mM and TG from 1.0 to 0.7 mM (Figures 5A, B). This was likely mediated by the transient increase in glucose, which rose from 4.6 to 6.5 mM following the dextrose drink (Figure ​(Figure5C).5C). The anti-lypoytic effect of dextrose drinks was shorter than that of KE drinks as d-βHB concentrations were elevated for longer after KE drinks than glucose after dextrose drinks. Insulin increased to ~ 35 mU.ml−1 after both the meal and the dextrose drink, but also increased to 13 ± 2 mU.ml−1 when KE was consumed whilst fasted owing to the 15 g of glucose in the flavored drink used as a diluent (Figure ​(Figure5D5D).
For subjects completing the initial experiment (n = 15), the amount of d-βHB excreted in the urine increased with d-βHB intake, but was <1.5% of the total βHB ingested and was not different between matched doses of KE vs. KS (Figure ​(Figure1I).1I). There was no change in urine volume produced in different study conditions. Baseline urinary pH (5.7 ± 0.1) was unchanged by KE ingestion (pH 6.4 ± 0.2. p = 0.8 vs. baseline) but was significantly alkalinized by KS consumption (pH 8.5 ± 0.1. p < 0.001 vs. baseline) (Figure ​(Figure1J1J).

So I’ve been primarily on a Keto diet for almost 6 months. During this time, I have fine tuned a lot to get my ketone levels up (Eating more fat and less protein). Most recently, I have used blood measurements for my ketone levels and I fluctuate between .6 and 2.6. The higher readings I get on the days I workout in the morning (about 5 hours before I draw blood and take a reading). I don’t have any problems sticking to the diet. It only seems to get easier. I’ve also incorporated 16 hour fasts which also are becoming easier over time. My priority and motivation for doing a keto diet is first and foremost weight loss. So far I have lost 40 pounds and I need to lose about 20 more. I do however want to improve my performance (running) and strength (I am doing the Stronglifts 5×5 program now).
Calories do matter, even on a ketogenic diet. If you consume more calories than your body uses, you’re going to gain weight. Period. What you mean to say is that it’s very difficult to eat your entire day’s worth of calories on a ketogenic diet because fats are so satiating. This distinction is important to keep in mind for those who generally have a voracious appetite (like me).
For all studies, the area under the curve (AUC) of blood [βHB] was calculated using the trapezium rule. In Study 3, for each of the three drinks, the initial rate of d-βHB appearance was estimated using d-βHB concentrations at baseline and 30 min post-drink, and d-βHB elimination was estimated using the AUC between the post-drink peak (60 min) and trough (180 min) d-βHB concentrations, with a baseline correction to the value at 180 min.
77. Volek JS, Sharman MJ, Gomez AL, Scheett TP, Kraemer WJ. An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial pipemic responses compared with a low fat diet in normal weight, normolipidemic women. J Nutr. 2003;133(9):2756–61. [PubMed]
The keto-esters are more appropriate for delivering higher doses of BOHB, but with repeated dosing can push the limits of taste and GI tolerance. There has been fairly extensive research on a compound 3-hydroxybutyl 3-hydroxybutyrate that is converted via hydrolysis and liver metabolism to yield 2 molecules of ketones, presumably mostly D-BOHB (Clarke 2012 and 2014). In a study involving lean athletes, an approximate 50 gram dose raised blood BOHB levels to 3 mM after 10 min and reached 6 mM by 20 min. Submaximal exercise resulted in increased ketone disposal from 2 to 3 hours and contributed significantly to whole body energy use during exercise (Cox 2016). This product has been shown to significantly reduce appetite after a single dose (Stubbs 2018) but its effect on body weight in humans over a longer period of time has not been studied, nor has its effect on blood glucose control been reported in humans with type 2 diabetes. However a single dose prior to a glucose tolerance test in healthy humans reduced blood glucose area-under-curve by 11% and non-esterified fatty acid area-under-curve by 44% (Myette-Cote 2018).
Exogenous ketones don’t seem to improve high-intensity, glucose-intensive exercise, increasing fat burning during steady state exercise but dropping top-end high-intensity performance. Another study found that ketone dieters reduced 50-minute time trial performance in cyclists, though another group of researchers have criticized the methods. Even when a ketone ester didn’t improve performance in the shuttle run to exhaustion and 15 meter sprint repeats, it did reduce the drop in brain function following the exercise.

Administration of ketone supplementation significantly reduced blood glucose over the course of the study (Fig. 3a, b). MCT (5 g/kg) decreased blood glucose compared to control within 30 min which was sustained for 8 h at baseline and at week 1. MCT (10 g/kg) likewise decreased blood glucose within 30 min and lasted through the 12 h time point during weeks 2, 3, and 4. BMS + MCT (5 g/kg) lowered blood glucose compared to control from hours 1–8 only at week 1. BMS + MCT (10 g/kg) lowered blood glucose compared to control within 30 min and remained low through the 12 h time point at weeks 2, 3, and 4. Rats supplemented with BMS had lower blood glucose compared to control at 12 h in week 4 (10) (Fig. 3a). Administration of BD did not significantly change blood glucose levels at any time point during the 4-week study. KE (5 g/kg) significantly lowered blood glucose levels at 30 min for week 1, 2, 3, and 4 and was sustained through 1 h at weeks 2–4 and sustained to 4 h at week 3. (Fig. 3b).


The difference in peak blood d-βHB concentrations between matched amounts of βHB as ester or salts arose because the salt contained l-βHB, as the blood concentrations of d- plus l-βHB isoforms were similar for both compounds. It is unclear if kinetic parameters of KE and KS drinks would be similar if matched d-βHB were taken in the drinks. Unlike d-βHB, blood l-βHB remained elevated for at least 8 h following the drink, suggesting an overall lower rate of metabolism of l-βHB as urinary elimination of l-βHB was in proportion to plasma concentration. Despite similar concentrations of total βHB, breath acetone was ~50% lower following KS drinks compared to KE, suggesting fundamental differences in the metabolic fates of D- and L-βHB. These findings support both previous hypotheses (Veech and King, 2016) and experimental work in rats (Webber and Edmond, 1977), which suggested that the l-isoform was less readily oxidized than the d-isoform, and is processed via different pathways, perhaps in different cellular compartments. It seems that l-βHB is not a major oxidative fuel at rest, and may accumulate with repeated KS drinks. However, the putative signaling role of l-βHB in humans remains unclear. In rodent cardiomyocytes, l-βHB acts as a signal that modulates the metabolism of d-βHB and glucose, Tsai et al. (2006) although no differences in blood glucose were seen here. Furthermore, L-βHB can act as a cellular antioxidant, although to a lesser extent than D-βHB (Haces et al., 2008).

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).4
Glucose and BHB went down slightly throughout the effort and RQ fell, implying a high rate of fat oxidation. We can calculate fat oxidation from these data. Energy expenditure (EE), in kcal/min, can be derived from the VO2 and VCO2 data and the Weir equation. For this effort, EE was 14.66 kcal/min; RQ gives us a good representation of how much of the energy used during the exercise bout was derived from FFA vs. glucose—in this case about 87% FFA and 13% glucose. So fat oxidation was approximately 12.7 kcal/min or 1.41 g/min. It’s worth pointing out that “traditional” sports physiology preaches that fat oxidation peaks in a well-trained athlete at about 1 g/min. Clearly this is context limited (i.e., only true, if true at all, in athletes on high carb diets with high RQ). I’ve done several tests on myself to see how high I could push fat oxidation rate. So far my max is about 1.6 g/min. This suggests to me that very elite athletes (which I am not) who are highly fat adapted could approach 2 g/min of fat oxidation. Jeff Volek has done testing on elites and by personal communication he has recorded levels at 1.81 g/min. A very close friend of mine is contemplating a run at the 24 hour world record (cycling). I think it’s likely we’ll be able to get him to 2 g/min of fat oxidation on the correct diet.

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