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!
Personally, I think it is wise to include a regular carb meal in your diet if you are going to follow a ketogenic diet. Long term ketogenic diets do seem to downregulate your thyroid and metabolism, and a weekly carb meal (or carb day) can help avoid this. The Carb Nite diet by J. Kiefer is a good example of this. And BJJCaveman posted his labs showing how a weekly carb meal helped his thyroid HERE.
There have been studies done on long term ketogenic diets. This 2004 paper inn Experimental & Clinical Cardiology titled ‘Long-term effects of a ketogenic diet in obese patients’ concluded that obese patients following a ketogenic diet for 24 ‘reduced the body weight and body mass index of the patients. Furthermore, it decreased the level of triglycerides, LDL cholesterol and blood glucose, and increased the level of HDL cholesterol. Administering a ketogenic diet for a relatively longer period of time did not produce any significant side effects in the patients. Therefore, the present study confirms that it is safe to use a ketogenic diet for a longer period of time than previously demonstrated.’
For the first part of my experiment, I would simply record my blood ketone and glucose levels over a period of two hours after taking the ketone esters. While I am already fairly keto-adapted and can attain nutritional ketosis fairly easily (> 0.5 mmol/L), it wasn’t until the end of my Five-day Fasting Mimicking Diet that I was even close to reaching therapeutic ketosis levels (>5.0 mmol/L).
Ketogenesis is the metabolism of fatty acids by β-oxidation. 4 This process gives acetyl CoA which then leads to β-hydroxy-β-methyglutaryl-CoA (HMG-CoA) as seen below5. HMG-CoA converts into Acetoacetone which can switch back and forth to BHB. Acetoacetone to Acetone conversion is irreversible (on the left below). Acetoacetate and BHB (via acetoacetate) are used to produce energy when converted back into acetyl-CoA within a cell’s mitochondria whilst Acetone is excreted in the breath and urine.4
Ketones are also a cleaner-burning fuel than carbs. They’re burned for energy in the mitochondria, and fewer free radicals (a highly-reactive, short-lived uncharged molecule) are generated when compared to burning glucose.15 What’s more, ketone molecules themselves cause a decrease in production of free radicals,21,22 while also increasing glutathione–a powerful antioxidant protecting against mitochondrial damage induced by free radicals.23
Blood, urine, plasma, and breath ketone concentrations following mole-matched ketone ester or isocaloric dextrose drinks in fed and fasted subjects (n = 16) at rest. Data from both of the two study visits in each condition (fed and fasted) completed by an individual are included in the analysis. Values are means ± SEM. (A) Blood d-βHB. (B) AUC of blood d-βHB. (C) Urine d-βHB excretion. (D) Plasma acetoacetate (AcAc). (E) Measured breath acetone (ppm = parts per million). (F,G) Mean d-βHB Cmax and difference between βHB Cmax over two visits when subjects separately consumed two ketone ester drinks in both the fed (F) and fasted (G) state. X axis = mean d-βHB Cmax of the 2 visits (mM), Y axis = difference between d-βHB Cmax in each visit. 95% confidence limits are shown as dotted lines. Significance denoted by: *p < 0.05 fed vs. fasted.
Over five visits, participants (n = 16) consumed either 4.4 mmol.kg−1 of βHB (2.2 mmol.kg−1 or 395 mg/kg of KE; 1 mole of KE delivered 2 moles of d-βHB equivalents): twice whilst fasted, and twice following a standardized meal, or an isocaloric dextrose drink without a meal. To improve palatability, drinks were diluted to 500 ml with a commercially available, citrus flavored drink containing 65 kCal (5 g of carbohydrate) (Glaceau, UK). The dextrose drink was taste-matched using a bitterness additive (Symrise, Holzminden, Germany). The standard meal consisted of porridge oats (54 g), semi-skimmed milk (360 ml) and banana (120 g), giving 600 kCal per person, with a macronutrient ratio of Carbohydrate: Protein: Fat of 2:1:1.
The two compounds commonly referred to as ‘ketone bodies’ (BOHB and AcAc) are produced and used for multiple purposes across nature from algae to mammals, but seldom in concentrations useful for extraction as human food. For this reason, the source of most exogenous ketones is chemical synthesis. Furthermore, most current research and use of ketone supplements focuses on BOHB. That is because AcAc is chemically unstable – it slowly breaks down to form acetone by releasing of one molecule of CO2.
I don’t think we even need a drumroll here… Based on my background research into ketone-supplement companies, the survey of Diet Doctor users and the experiment itself, we cannot recommend taking these supplements. I can personally think of many more beneficial ways to invest money in my health, such as buying grass-fed meat and organic vegetables, or even buying a bicycle and riding it outside in the sunshine.
Another important difference between endogenous and exogenous BOHB is that most synthetic BOHB used in dietary supplements is a mixture of the two ‘D’ and ‘L’ isomers, whereas endogenously produced BOHB consists of just the D-isomer. Metabolically, the two isomers are very different, and current published information indicates that most of the energy and signaling benefits of BOHB derive from the D-form. This is potentially problematic because the L-isomers are not metabolized via the same chemical pathways as the D-forms (Lincoln 1987, Stubbs 2017), and it remains unclear whether humans can convert the L-form to the D-form.
Blood d-βHB, pH, bicarbonate (HCO3-) and electrolytes measured in arterialized blood samples from resting subjects (n = 7) following a ketone ester or salt drink containing 3.2 mmol.kg−1 of βHB. Shaded areas represent the normal range. Values are means ± SEM. (A) Venous blood d-βHB. (B) Arterialized blood pH. (C) Blood bicarbonate. (D) Blood potassium. (E) Blood sodium. (F) Blood chloride. †p < 0.05 difference between KE and KS, *p < 0.05 difference from baseline value.
The concentrations of blood d-βHB after KE drinks were highly repeatable whether consumed whilst fasted or fed (Figures 4F,G). The d-βHB Cmax values ranged from 1.3 to 3.5 mM when fed and 2.3 to 4.7 mM when fasted. There was no significant effect of visit order on d-βHB kinetics, with the maximal difference in d-βHB Cmax reached by one individual being 1.2 mM when fed and 1.9 mM when fasted. Approximately 61% of the variation in the data was attributable to feeding (fed vs. fasted), <1% to visit order, 16% to inter-participant variability, and the residual 24% variability due to non-specific random effects.
I have tried the following preparations of exogenous ketones: BHB monoester, AcAc di-ester, BHB mineral salt (BHB combined with Na+, K+, and Ca2+). I have consumed these at different concentrations and in combination with different mixing agents, including MCT oil, pure caprylic acid (C8), branch-chained amino acids, and lemon juice (to lower the pH). I won’t go into the details of each, though, for the sake of time.
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