Slowly ramp up your ketone intake. Be patient! 🙂 For many of us, our bodies aren’t used to running on ketones, so you can expect an adjustment period. Try ¼ scoop first. Transitioning to ketosis removes water from our bodies, so getting lots of water will help with any dehydration and stomach issues. Ramp up from there, trying ½ scoop the second week or when you feel it’s appropriate, and then try a whole scoop 1-2 weeks in. You can use it for extra energy or to help get into ketosis if you aren’t there already. Most people use it 0-3 times per day.
Hello! I’m planning on taking a short vacation and will be having “kept friendly” drinks, mostly vodka and water with lemon and stevia. When should I take my exogenous ketones? That night before bed or early the next morning or after the 3 day vacation is completely over? I’m unsure how to manage this to have the best odds of staying in ketosis and get back to burning FAT. Also, I just purchased Instaketones from Julian Bakery, what are your thoughts on this brand? Thanks for what you do!
There’s debate raging about which dietary tactic is the god particle for making you leaner, faster and healthier. How the ketogenic diet option squares off against the low carb route is vital for understanding the ways in which exogenous ketone supplements work. To get into ketosis the natural way, you need to keep your carb intake low enough for long enough for your body to begin using use fat as fuel. Your liver then converts a portion of that fat into energy molecules called ketones. These work together with glucose as a fuel source, but can actually kick in faster, allowing your body to operate more economically during lengthy, high-energy exercise efforts.
As ketone drinks can deliver nutritional ketosis without fasting, we investigated the effect of food on KE uptake and metabolism. It is well documented that food in the gut can slow, or prevent, the uptake of small hydrophilic hydrocarbons, such as βHB (Melander, 1978; Toothaker and Welling, 1980; Horowitz et al., 1989; Fraser et al., 1995), so decreased gut βHB uptake is probably the cause of lower blood βHB following the meal. Despite higher blood βHB concentrations in the fasted state, the meal did not alter plasma AcAc. This suggests that the rate of conversion of βHB to AcAc may not match the rate of appearance of βHB following KE consumption. Alternatively, meal-induced changes in the hepatic ratio of NAD+:NADH may have altered the conversion of βHB to AcAc (Himwich et al., 1937; Desrochers et al., 1992).
Once you hit the bed, the adrenal glands will be off and the body will enter the anabolic stage. This will allow your body to repair itself. If you stay up late for long periods of time your body will enter the hypercatabolic state. In this state, the levels of cortisol in your body increase significantly. This also increases the insulin resistance of the body which would again increase the blood sugar levels.
Ketone monoester and diester compounds may circumvent the problems associated with inorganic ion consumption in KS drinks. KE ingestion rapidly increased blood ketone concentrations to >5 mM in animals (Desrochers et al., 1995a,b; Clarke et al., 2012a) and the first oral, non-racemic KE for human consumption, (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, raised blood βHB concentrations to 3–5 mM in healthy adults (Clarke et al., 2012b; Shivva et al., 2016) and athletes (Cox et al., 2016; Holdsworth et al., 2017; Vandoorne et al., 2017). However, the pharmacokinetics and pharmacodynamics of this KE with confounding factors, such as prandial state or multiple KE drinks, have not been characterized.
In addition to the Weir coefficients being potentially off (which impacts EE), the RQ interpretation may be incorrect in the presence of endogenous or exogenous ketones. As a result, the estimation of fat and glucose oxidation may be off (though it’s directionally correct). That said, the current interpretation seems quite plausible—greater fat oxidation when I had to make my ketones; less when I got my ketones for “free.”
Ketogenic Diets and Physical Performance – Impaired physical performance is a common but not obligate result of a low carbohydrate diet. Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15–25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis.
Here we investigated the effects of KE and KS consumption on blood βHB and metabolite concentrations. As we found that KE ingestion delivered a >50% higher plasma concentrations of d-βHB alone, we subsequently determined the reliability and repeatability of ketosis following KE consumption and the effects of concomitant meal ingestion on blood ketone and substrate kinetics. Finally, we determined whether nasogastric infusion could be used for KE administration, given that some patients require feeding in this manner.
First and foremost, one of the most important factors is to be discipline when following the ketogenic diet. This means heavily restricting your carbohydrate intake, while switching to high-fat foods and moderate proteins. The general rule of thumb when it comes to splitting your macros out should look something like this: 5% (carbs)/ 80% (fats)/ 15% (proteins). Although if you’re just starting out, I wouldn’t focus too heavily on macros but rather place more importance in restricting your carbohydrate intake to 20 grams or less. Depending on the individual, most keto diets will allow approximately 20g-70g of net carbs as part of your overall daily intake, but if you’re asking the extreme question of ‘how to get into ketosis in 24 hours?’ then let’s focus on the absolute limit. For a more detailed breakdown, please see my keto shopping list article.
Exogenous ketones (also known as ketone supplements) and well-formulated ketogenic diets share at least one thing in common. They both result in increased circulating concentrations of beta-hydroxybutyrate (BOHB), but ultimately are associated with very different patterns of ketosis, as well as differing metabolic and physiologic outcomes. In short, they should not be assumed to have equivalent effects simply because they achieve similar BOHB blood levels. Having said that, there are many reasons we should continue to study the various forms and potential applications of ketone supplements.
Over four visits, participants (n = 15) consumed 1.6 and 3.2 mmol.kg−1 of βHB as KE (141 mg/kg and 282 mg/kg of R-3-hydroxybutyl-R-1,3-hydroxybutyrate) or as KS (KetoForce, KetoSports, USA) sodium and potassium βHB, containing 1.6–3.2 g of each cation), plus 6 g of sweetener containing 19 kCal (4 g of carbohydrate) (Symrise, Holzminden, Germany), diluted to 300 ml using water. Drink blinding was not possible due to unmaskable differences in taste (bitter vs. salty).
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).
The ketone esters are, hands-down, the worst tasting compounds I have ever put in my body. The world’s worst scotch tastes like spring water compared to these things. The first time I tried 50 mL of BHB monoester, I failed to mix it with anything (Dom warned me, but I was too eager to try them to actually read his instructions). Strategic error. It tasted as I imagine jet fuel would taste. I thought I was going to go blind. I didn’t stop gagging for 10 minutes. (I did this before an early morning bike ride, and I was gagging so loudly in the kitchen that I woke up my wife, who was still sleeping in our bedroom.) The taste of the AcAc di-ester is at least masked by the fact that Dom was able to put it into capsules. But they are still categorically horrible. The salts are definitely better, but despite experimenting with them for months, I was unable to consistently ingest them without experiencing GI side-effects; often I was fine, but enough times I was not, which left me concluding that I still needed to work out the kinks. From my discussions with others using the BHB salts, it seems I have a particularly sensitive GI system.
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