Onnit is an incredible company that’s making a massive impacts in the lives of athletes in nearly every sport. From Olympic Gold Medalists, to NFL middle linebackers, Onnit has taken athletic performance to a new level. Providing supplements, food, and training equipment, Onnit was an early adopter of the elite performance booster that is exogenous ketones!


We are told by our parents, doctors, and the media that milk builds strong bones and that we should take calcium supplements to help protect against osteoporosis. Indeed, calcium deficiency can lead to a plethora of health problems[12]. However, those of us who take calcium supplements or consume calcium-fortified foods and beverages may, in fact, be consuming above the Recommended Dietary Allowance (RDA) of calcium.
North Americans typically live pro-inflammatory, pro-disease lives (think about your everyday: likely sitting in a flexed position for hours on end, not enough natural sunlight, not enough movement, artificial food stuffs, artificial colouring, going to bed late, blue light exposure, less in-person contact with our loved ones, late night snacks, the list goes on and on).
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.
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.
Ketone Esters: These are not normally found in the body, but exogenous ketone esters convert into BHB once it is in the body. They are also synthetically (lab) made compounds that link an alcohol to a ketone body, which can then be metabolized by the liver into a ketone. They are like ketone salts on steroids as they have 5-10 time more BHB per serving/maximum daily intake than ketone salts. To date, pure ketone esters have been very expensive to produce and have only been available to researchers, elite athletes (Tour de France cyclists), and the US Department of Defense (people have spent more than $20,000 to have an independent lab produce a single serving!).

Look around your grocery store, and you’ll soon start to see “Fortified with Calcium” on a variety of different labels, along with calcium supplements everywhere you look. Calcium is essential for cardiovascular health, but several studies have found too much calcium to be associated with cardiovascular events and even death.  One study found that consumption of 1000+ mg of supplemental calcium per day was associated with an increased risk of death from cardiovascular disease in men but not women[13]. Dietary calcium intake (i.e., calcium from incorporated foods such as milk, etc.), on the other hand, was not associated with death from cardiovascular disease in men or women. Additionally, a different study found 1000 mg of supplemental calcium to be associated with an increase in rates of cardiovascular events in women[14].


I heard a rep from Perfect Keto on a podcast and your Exogenous Ketones. I ordered and received it the other day. I see from this article that I should not do a full scoop at once, but break it up in a day. Good to know. I had about a half scoop before I worked out this morning and could tell I had more energy. Loved that. Just curious….any ideas how long it will take me to get back into ketosis and fat burning?? (I know it depends on what I eat, but a general idea that I promise not to hold you too! (I’m actually missing having ‘keto breath!)
If you noticed that you're not getting into ketosis quick enough, chances are you're not eating enough fat. Eating plenty of healthy fat is essential in inducing ketosis. One reason why this is so is that your body makes ketones from fat. The other reason being that fat is highly satiating, so your body won't slow down or start breaking down muscle for fuel.
I’m often asked if it’s necessary to buy and use keto products like urine sticks. They’re small test strips that you dip in urine to see if your body is producing ketones (and therefore indicate if you’ve entered ketosis.) There's very little information on how to know that you are in ketosis other than using these ketones supplements because they are as accurate as can be in determining your current state. Outside of that, you can only guess if you are in it or not by your body's performance.
Over the 28-day experiment, ketone supplements administered daily significantly elevated blood ketone levels without dietary restriction (Fig. 2a, b). Naturally derived ketogenic supplements including MCT (5 g/kg) elicited a significant rapid elevation in blood βHB within 30–60 min that was sustained for 8 h. BMS + MCT (5 g/kg) elicited a significant elevation in blood βHB at 4 h, which was no longer significant at 8 h. BMS (5 g/kg) did not elicit a significant elevation in blood βHB at any time point. For days 14–28, BMS + MCT (10 g/kg) and MCT (10 g/kg) elevated blood βHB levels within 30 min and remained significantly elevated for up to 12 h. We observed a delay in the peak elevation of blood βHB: BMS + MCT peaked at 8 h instead of at 4 h and MCT at 4 h instead of at 1 h. Blood βHB levels in the BMS group did not show significant elevation at any time point, even after dose escalation (Fig. 2a). Synthetically derived ketogenic supplements including KE and BD supplementation rapidly elevated blood βHB within 30 min and was sustained for 8 h. For the rats receiving ketone supplementation in the form of BD or the KE, dosage was kept at 5 g/kg to prevent adverse effects associated with hyperketonemia. The Precision Xtra™ ketone monitoring system measures βHB only; therefore, total blood ketone levels (βHB + AcAc) would be higher than measured. For each of these groups, the blood βHB profile remained consistent following daily ketone supplementation administration over the 4-week duration. (Fig. 2b).

One common concern regarding the KD is its purported potential to increase the risk of atherosclerosis by elevating blood cholesterol and triglyceride levels [55, 56]. This topic remains controversial as some, but not all, studies have demonstrated that the KD elevates blood levels of cholesterol and triglycerides [57–62]. Kwitervich and colleagues demonstrated an increase in low-density lipoprotein (LDL) and a decrease in high-density lipoprotein (HDL) in epileptic children fed the classical KD for two years [27]. In this study, total cholesterol increased by ~130 %, and stabilized at the elevated level over the 2-year period. A similar study demonstrated that the lipid profile returned to baseline in children who remained on the KD for six years [63]. Children typically remain on the diet for approximately two years then return to a diet of common fat and carbohydrate ingestion [64]. The implications of these findings are unclear, since the influence of cholesterol on cardiovascular health is controversial and macronutrient sources of the diet vary per study. In contrast to these studies, the majority of recent studies have suggested that the KD can actually lead to significant benefits in biomarkers of metabolic health, including blood lipid profiles [65–72]. In these studies, the KD positively altered blood lipids, decreasing total triglycerides and cholesterol while increasing the ratio of HDL to LDL [68–77]. Although, the KD is well-established in children, it has only recently been utilized as a strategy to control seizures in adults. In 2014, Schoeler and colleagues reported on the feasibility of the KD for adults, concluding that 39 % of individuals achieved > 50 % reduction in seizure frequency, similar to the results reported in pediatric studies. Patients experienced similar gastrointestinal adverse advents that have been previously described in pediatric patients, but they did not lead to discontinuation of the diet in any patient [78].
The other potentially important distinction between nutritional ketosis and chemically-induced ketosis is the potential metabolic role played by liver AcAc production and redox status. Although the ratio of BOHB to AcAc in venous blood is typically 80% to 20%, classic studies by Cahill (1975) have observed important hepatic vein and peripheral arterio-venous gradients for this ratio in keto-adapted patients. What these observations imply is that the liver produces a higher proportion of AcAc than is found in the peripheral blood, and that this is due to uptake of AcAc in peripheral cells (principally muscle) with re-release as BOHB. In the process, the reduction of AcAc to BOHB produces NAD+, which is beneficial to mitochondrial redox state and mitochondrial function (Verdin 2015, Newman 2017).
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].

Satiety decreased in both cases, slightly less with the supplements than with the placebo: participants reported feeling less hungry after taking the supplements than after taking the placebo. However, we are doubtful whether this would be enough of a difference to impact food intake and therefore induce weight loss indirectly, compared to not taking a supplement at all. Especially since, as noted before, BHB switches off lipolysis.


More tolerable than MCT oil: MCT oil has been known to cause gastrointestinal distress in users, especially when taken in higher amounts. Exogenous ketones in the form of ketone salts, in comparison, are well-tolerated. Thus they enable one to avoid adverse GI events while providing the body with similar types of benefits. Figure 2 shows Ketone esters can be effective at reducing appetite. A combination of MCT oil and exogenous ketones may aid weight loss and allow a lower loading of ketone supplements, without the GI distress seen with MCT oil.
After a minimal amount of internet "research," I decided to try my first exogenous ketones. I have used the ketogenic diet off and on for at 15 years and my body is pretty efficient at fat adapting. (Usually by the end of 2 strict days, I am in ketosis, but not without symptoms and intense cravings.) I can consistently fast from carbs for 20 - 24 hours and do this consistently. However, around hour 20, my mind begins to negotiate that intermittent fasting is advantageous too and that I can afford to have some carbs once a day. Hence the yo-yo effect.

Recent studies suggest that many of the benefits of the KD are due to the effects of ketone body metabolism. Interestingly, in studies on T2D patients, improved glycemic control, improved lipid markers, and retraction of insulin and other medications occurred before weight loss became significant. Both βHB and AcAc have been shown to decrease mitochondrial reactive oxygen species (ROS) production [36–39]. Veech et al. have summarized the potential therapeutic uses for ketone bodies [28, 40]. They have demonstrated that exogenous ketones favorably alter mitochondrial bioenergetics to reduce the mitochondrial NAD couple, oxidize the co-enzyme Q, and increase the ΔG’ (free enthalpy) of ATP hydrolysis [41]. Ketone bodies have been shown to increase the hydraulic efficiency of the heart by 28 %, simultaneously decreasing oxygen consumption while increasing ATP production [42]. Thus, elevated ketone bodies increase metabolic efficiency and as a consequence, reduce superoxide production and increase reduced glutathione [28]. Sullivan et al. demonstrated that mice fed a KD for 10–12 days showed increased hippocampal uncoupling proteins, indicative of decreased mitochondrial-produced ROS [43]. Bough et al. showed an increase of mitochondrial biogenesis in rats maintained on a KD for 4–6 weeks [44, 45]. Recently, Shimazu et al. reported that βHB is an exogenous and specific inhibitor of class I histone deacetylases (HDACs), which confers protection against oxidative stress [38]. Ketone bodies have also been shown to suppress inflammation by decreasing the inflammatory markers TNF-a, IL-6, IL-8, MCP-1, E-selectin, I-CAM, and PAI-1 [8, 46, 47]. Therefore, it is thought that ketone bodies themselves confer many of the benefits associated with the KD.
My two cents: I wouldn’t take ketone supps if not on some sort of low(ish) carb diet because the idea of high levels of BOTH fuels (ie, ketones AND glucose) doesn’t seem physiologically appropriate… more like a recipe for disaster, and by “disaster,” I mean “out-of-control production of Reactive Oxygen Species” — this might not matter if you’re an athlete looking for a quick performance boost, because the fuels are going to be cleared rather quickly… not so much if you’re a desk jockey.
Proper sleep is important for hormone function and repair of the body. Not getting enough sleep is tough on the adrenals and blood sugar regulation. Try to get at least seven hours of sleep per night. If you struggle with quality sleep, create an environment that is conducive for rest. This could be keeping your room cooler, turning off all electronic devices one to two hours before bedtime or using a sleep mask.
When your body transitions from using energy from carbohydrates to ketones, there can be a lot of nasty and unwanted side effects. These include low energy, bloating, irritability, headaches and fatigue. This is because your body is “in between” burning carbs and burning ketones and hasn’t become efficient at burning ketones and producing them from your fat stores yet.

Several studies have investigated the safety and efficacy of ketone supplements for disease states such as AD and Parkinson’s disease, and well as for parenteral nutrition [40, 48–50, 100–103]. Our research demonstrates that several forms of dietary ketone supplementation can effectively elevate blood ketone levels and achieve deleted: therapeutic nutritional ketosis without the need for dietary carbohydrate restriction. We also demonstrated that ketosis achieved with exogenous ketone supplementation can reduce blood glucose, and this is inversely associated with the blood ketone levels. Although preliminary results are encouraging, further studies are needed to determine if oral ketone supplementation can produce the same therapeutic benefits as the classic KD in the broad-spectrum of KD-responsive disease states . Additionally, further experiments need to be conducted to see if the exogenous ketone supplementation affects the same physiological features as the KD (i.e. ROS, inflammation, ATP production). Ketone supplementation could be used as an alternative method for inducing ketosis in patients uninterested in attempting the KD or those who have previously had difficulty implementing the KD because of palatability issues, gall bladder removal, liver abnormalities, or intolerance to fat. Additional experiments should be conducted to see if ketone supplementation could be used in conjunction with the KD to assist and ease the transition to nutrition ketosis and enhance the speed of keto-adaptation. In this study we have demonstrated the ability of several ketone supplements to elevate blood ketone levels, providing multiple options to induce therapeutic ketosis based on patient need. Though additional studies are needed to determine the therapeutic potential of ketone supplementation, many patients that previously were unable to benefit from the KD may now have an alternate method of achieving therapeutic ketosis. Ketone supplementation may also represent a means to further augment ketonemia in those responsive to therapeutic ketosis, especially in those individuals where maintaining low glucose is important.
Again, there are very interesting animal studies plus some single case reports and small uncontrolled trials of humans with neurodegenerative disease and cancer given ketogenic diets and/or exogenous ketones (Murray 2016, Poff 2015, Roberts 2017, Newport 2015, Cunnane 2016). In some cases where the patient does not have the cognitive resources to comply with a well-formulated ketogenic diet, or where target blood levels of BOHB that work in animals are hard to achieve in humans by diet alone, supplemental ketones may have an important role to play in the prevention, management, or reversal of these disease categories.
My two cents: I wouldn’t take ketone supps if not on some sort of low(ish) carb diet because the idea of high levels of BOTH fuels (ie, ketones AND glucose) doesn’t seem physiologically appropriate… more like a recipe for disaster, and by “disaster,” I mean “out-of-control production of Reactive Oxygen Species” — this might not matter if you’re an athlete looking for a quick performance boost, because the fuels are going to be cleared rather quickly… not so much if you’re a desk jockey.
The “BHB salt” is simply a compound that consists of sodium (Na+), potassium (K+), and the ketone body β-hydroxybutyrate.  In supplements like Pruvit’s Keto OS  these individual components are being held together by ionic bonds; however, when you consume the product, it is absorbed into the blood where it dissociates into free Na+, K+, and BHB since it is a water-based solution.  Thus, consuming the product directly and immediately puts more ketones into your blood.
I have, though, recently been diagnosed with ovarian cancer. After reading through your blog, I noticed there was a little about Ketogenetic diet and cancer. I purchased the MCT oil powder in hopes that will help me get into ketosis for the purpose of “starving” the cancer cells. Other then focus, I didn’t see any particular format for something like this. Here are my questions: How much of the powder should I take? And do you think the diet plus the MCT oil is a good idea for 1) aiding chemotherapy and 2) helping shrink the number of cancer cells?
This is probably one of the most understood notions of a true ketogenic diet (and the difference between a keto diet and a low carb diet). An optimal ketogenic diet will be low in carbohydrates AND protein. Many people who have experimented with low carb dieting simple reduce carbs and increase protein. A big reason behind this is due to the misconception that ‘’excess fat is bad – which is untrue, more on this HERE). However, excess protein can be converted to glucose (blood sugar) through a process called gluconeogenesis.
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.
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.”

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