The classical KD consists of a 4:1 ratio of fat to protein and carbohydrate, with 80–90 % of total calories derived from fat [27]. The macronutrient ratio of the KD induces a metabolic shift towards fatty acid oxidation and hepatic ketogenesis, elevating the ketone bodies acetoacetate (AcAc) and β-hydroxybutyrate (βHB) in the blood. Acetone, generated by decarboxylation of AcAc, has been shown to have anticonvulsant properties [28–32]. Ketone bodies are naturally elevated to serve as alternative metabolic substrates for extra-hepatic tissues during the prolonged reduction of glucose availability, suppression of insulin, and depletion of liver glycogen, such as occurs during starvation, fasting, vigorous exercise, calorie restriction, or the KD. Although the KD has clear therapeutic potential, several factors limit the efficacy and utility of this metabolic therapy for widespread clinical use. Patient compliance to the KD can be low due to the severe dietary restriction - the diet being generally perceived as unpalatable - and intolerance to high-fat ingestion. Maintaining ketosis can be difficult as consumption of even a small quantity of carbohydrates or excess protein can rapidly inhibit ketogenesis [33, 34]. Furthermore, enhanced ketone body production and tissue utilization by the tissues can take several weeks (keto-adaptation), and patients may experience mild hypoglycemic symptoms during this transitional period [35].
It might sound absolutely crazy to go that long without food. Especially when you consider traditional diets that recommend eating 3-5 small meals each day, starting with breakfast – the “most important” meal of the day. But if you think back to hunter gatherer times, human beings didn’t always have food accessible to us. Farming and agriculture hadn’t existed so our first meal each day would vary quite vastly. If you think about the word itself, ‘breakfast’ means to break-fast. We didn’t have a set time where we would consume our first meal – it was dependent on accessibility. So if you’re wondering how you’re going to survive without going for food for 16 hours, the answer is straight forward – you can! Let’s simplify this and break down what this may potentially look like.
In conclusion, drinks containing exogenous ketones, in either ester or salt form, can raise concentrations of blood βHB in humans, although elevation of l-βHB lasts longer after racemic KS consumption. Both KE and KS drinks mildly altered acid-base balance. Exogenous ketones lowered blood glucose and lipids without inhibiting endogenous insulin secretion. The KE delivered highly repeatable blood concentrations of d-βHB, although ketosis was decreased by a meal. Uptake and elimination of d-βHB were similar when several drinks were consumed in succession. The dietary KE could maintain ketosis using drinks taken regularly around a normal meal pattern, or using a continuous infusion via a nasogastric tube. Therefore, ketone drinks are a viable and practical alternative to dietary strategies to achieve ketosis.
These studies were approved by external Research Ethics Committees (London Queen's Square: 14/LO/0288 and South West Frenchay: 15/SW/0244) and were conducted in accordance with the Declaration of Helsinki (2008). Studies took place at the University of Oxford between September 2014 and September 2016. Participants were healthy, aged 21–57, non-smokers and had no history of major illness. Female participants were using oral contraception to minimize the effects of menstrual phase on results. Participants provided written informed consent prior to inclusion, and completed a confidential medical screening questionnaire to determine eligibility. Anthropometric characteristics are shown in Table ​Table1.1. Sample sizes were chosen following an estimated power calculation based on the effect size in previous work using KE drinks (Clarke et al., 2012b; Shivva et al., 2016).

Effects of beta-hydroxybutyrate on cognition in memory-impaired adults. – Glucose is the brain’s principal energy substrate. In Alzheimer’s disease (AD), there appears to be a pathological decrease in the brain’s ability to use glucose. Neurobiological evidence suggests that ketone bodies are an effective alternative energy substrate for the brain. Elevation of plasma ketone body levels through an oral dose of medium chain triglycerides (MCTs) may improve cognitive functioning in older adults with memory disorders. On separate days, 20 subjects with AD or mild cognitive impairment consumed a drink containing emulsified MCTs or placebo. Significant increases in levels of the ketone body beta-hydroxybutyrate (beta-OHB) were observed 90 min after treatment (P=0.007) when cognitive tests were administered. beta-OHB elevations were moderated by apolipoprotein E (APOE) genotype (P=0.036). For 4+ subjects, beta-OHB levels continued to rise between the 90 and 120 min blood draws in the treatment condition, while the beta-OHB levels of 4- subjects held constant (P<0.009). On cognitive testing, MCT treatment facilitated performance on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-cog) for 4- subjects, but not for 4+ subjects (P=0.04). Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02). Additional research is warranted to determine the therapeutic benefits of MCTs for patients with AD and how APOE-4 status may mediate beta-OHB efficacy. (

Also known as the carb flu, the keto flu is commonly experienced by people who are transitioning to a Ketogenic diet. “Keto flu” is not actually flu but mimics the experience of flu with very similar symptoms. It can happen when someone who has become accustomed to relying primarily on carbohydrates as fuel removes them from their diet. Whilst this is a necessary step towards adjusting from being a sugar-burner to a fat-burner, the sudden change can trigger some unpleasant symptoms, much like withdrawing from an addictive substance. Keto flu symptoms can include drowsiness, nausea, dizziness, achy muscles, mental fogginess and an irritable mood. The good news though, is that most of these experiences relate to dehydration and electrolyte depletion, and so are easily prevented or managed. Simply adding a ¼ - ½ teaspoon of a high quality sea salt or sodium/potassium powder to a glass of water works wonders; however you may still require a separate magnesium supplement; particularly if you are prone to muscle cramps or restless legs. Another popular way to manage your electrolytes is via a good quality bone broth powder. Finally, since BHB’s are normally delivered via a mineral salt base*, keto flu symptoms are easily prevented or reduced by using an exogenous ketone supplement powder.

When your body is done using up a certain substrate to create energy (acetyl-CoA) after eating carbohydrates, it will start to find creative ways to get the job done. This is something that you want to happen. This is the switch to ketosis. If you didn’t do this, you’d be dead after fasting for a very short period of time. Under normal circumstances, the liver will start making beta-hydroxybutyrate from long chain and medium chain fatty acids that are liberated from your fat tissue. You are turning fat into fuel. Good work. This is why people can fast for months at a time and still function like normal humans.
d-βHB was measured immediately on whole blood using a handheld monitor and enzyme-based reagent strips (Precision Xtra, Abbott Diabetes Care, UK). Samples were stored on ice, centrifuged and duplicate plasma aliquots stored at −80°C. All urine passed during the visit was collected, the total volume recorded, and 1 ml aliquots taken, frozen and retained for analysis.
Let’s briefly discuss some organic chemistry. Two molecules that are “the same” but mirror images of each other (like your hands) are known as enantiomers, a type of spatial isomer. Beta hydroxybutyrate comes in two forms, D-β-hydroxybutyrate (“right-handed”) and L-β-hydroxybutyrate (“left-handed”). D-β-hydroxybutyrate is the form that is naturally produced in the body and is most bioavailable when taken exogenously.
Baseline measurements showed no significant changes in triglycerides or the lipoproteins (data not shown). Data represent triglyceride and lipoprotein concentrations measured after 4 weeks of daily exogenous ketone supplementation. No significant change in total cholesterol was observed at 4 weeks for any of the ketone treatment groups compared to control. (Fig. 1a). No significant difference was detected in triglycerides for any ketone supplement compared to control (Fig. 1b). MCT supplemented animals had a significant reduction in HDL blood levels compared to control (p < 0.001) (Fig. 1c). LDL levels in ketone-supplemented animals did not significantly differ from controls (Fig. 1d).
Increased calcium levels in the bloodstream may contribute to the hardening of arteries (atherosclerosis), which in turn can lead to a heart attack.  Calcium from supplements enters the bloodstream in one bolus, whereas we usually tend to get calcium from foods in small doses from the breakdown process. This might explain why calcium from food doesn’t create the same risk that is introduced by calcium supplements. At first glance, it seems to be the case that high calcium intake –at least from supplements–may not be ideal.
Directions — — As a dietary supplement, mix 1 scoop of ketone powder with 8-12 oz of water To avoid gastrointestinal discomfort, start with 1/2 scoop (or even less) and gradually increase to a full serving. Best consumed prior to exercise to enhance performance. Do not exceed 3 scoops per day. As a dietary supplement take 1 serving of PX Ketotropin twice daily. Ideally the 1st servings (4 capsules) should be taken prior to the first meal of the day. Consume 2nd serving 30 minutes prior to strenuous physical activity. If no physical activity is performed please consumer 2nd serving prior to afternoon meal. Additional servings can be taken in between meals throughout the day if needed. Do not consume more than 6 servings of PX Ketotropin
Effects of ketone supplementation on triglycerides and lipoproteins: Ketone supplementation causes little change in triglycerides and lipoproteins over a 4-week study. Graphs show concentrations at 4-weeks of total cholesterol (a), Triglycerides (b), LDL (c), and HDL (d). MCT supplemented rats had signfiicantly reduced concentration of HDL blood levels compared to control (p < 0.001) (b). One-Way ANOVA with Tukey’s post hoc test, results considered significant if p < 0.05. Error bars represent mean (SD)

Over five visits, participants (n = 16) consumed either 4.4−1 of βHB (2.2−1 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.
I’m getting an increasing number of questions about exogenous ketones. Are they good? Do they work for performance? Is there a dose-response curve? If I’m fasting, can I consume them without “breaking” the fast? Am I in ketosis if my liver isn’t producing ketones, but my BOHB is 1.5 mmol/L after ingesting ketones? Can they “ramp-up” ketogenesis? Are they a “smart drug?” What happens if someone has high levels of both glucose and ketones? Are some products better than others? Salts vs esters? BHB vs AcAc? Can taking exogenous ketones reduce endogenous production on a ketogenic diet? What’s the difference between racemic mixtures, D-form, and L-form? What’s your experience with MCTs and C8?

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