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Exogenous ketones are becoming more popular as advancements in scientific research continue to show how they work to improve both health and performance. At first, the only options for delivering exogenous ketones were unpalatable ketone esters; however, exogenous ketones can now be taken in the form of ketone mineral salts that are more palatable and easily blended in water. Making ketone mineral salts involves combining beta-hydroxybutyrate (BHB) with mineral salts such as sodium, calcium, magnesium, or potassium. Before considering whether ketone supplements are a good option, most people immediately look at the salt load, and rightfully so. It is important to take into account the nutritional and health impact of not only the BHB but the minerals that are used to make the product.
Great information. And apparently I have found out what my problem is. I got into Keto a few weeks ago. Transitioned into ketosis after a week, and then had to travel….while I followed a keto diet as best I could, (I took your powdered MCT Oil with me and it is great), but I did fall out of ketosis. Now it’s been 2 weeks and I can’t seem to get back into ketosis.
Ketone Salts: While the body uses and makes BHB ketones salts naturally, in supplement form ketone salts are synthetically (lab) made compounds that combine sodium (and/or potassium, calcium, or magnesium) with BHB. The salt is used to raise the pH and make things less acidic. Currently, all ketone supplements on the market are made from ketone salts. While they raise ketone levels, most people will only experience mild nutritional ketosis (~0.6-1.0 mmol/L).
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.
Too low of sodium intake can be just as dangerous as getting too much. As with all essential nutrients, the graph for risk associated with sodium and health problems is actually u-shaped, such that both low and high quantities of sodium are associated with risk of cardiovascular disease and all-cause mortality. Evidence also suggests that restricting sodium to the recommendations may rapidly increase plasma levels of renin, angiotensin II, and aldosterone, which can lead to complications in itself.
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.
An alternative to the ketogenic diet is consumption of drinks containing exogenous dietary ketones, such as ketone esters (KE) and ketone salts (KS). The metabolic effects of KS ingestion have been reported in rats (Ari et al., 2016; Kesl et al., 2016; Caminhotto et al., 2017), in three extremely ill pediatric patients (Plecko et al., 2002; Van Hove et al., 2003; Valayannopoulos et al., 2011) and in cyclists (O'Malley et al., 2017; Rodger et al., 2017). However, the concentrations of blood βHB reached were low (<1 mM) and a high amount of salt, consumed as sodium, potassium and/or calcium βHB, was required to achieve ketosis. Furthermore, dietary KS are often racemic mixtures of the two optical isoforms of βHB, d-βHB, and l-βHB, despite the metabolism of l-βHB being poorly understood (Webber and Edmond, 1977; Scofield et al., 1982; Lincoln et al., 1987; Desrochers et al., 1992). The pharmacokinetics and pharmacodynamics of KS ingestion in healthy humans at rest have not been reported.
This is an excellent resource. Thank you for all the work and resources you found. i had never even heard of Adkins 72. I am keto but I always let Sunday be my high Carb cheat day.So im learning from this blog how to get back in ketosis in 24 hours after my 4pm meal on Sunday The Lords & family day. So im 25hr fasting. I would like to reference this article on my blog, thanks for helping me on my 100 lb lost journey.
Serial drinks or a continuous NG infusion of KE effectively kept blood ketone concentrations >1 mM for 9 h (Figure (Figure6).6). With drinks every 3 h, blood d-βHB rose and then fell, but had not returned to baseline (~ 0.1 mM) when the next drink was consumed. There was no significant difference in d-βHB Cmax between drinks 2 and 3 (3.4 ± 0.2 mM vs. 3.8 ± 0.2 mM p = 0.3), as the rate of d-βHB appearance fell slightly with successive drinks (0.07 ± 0.01 mmol.min−1 and 0.06 ± 0.01 mmol.min−1 p = 0.6). d-βHB elimination was the same after each bolus (142 ± 37 mmol.min, 127 ± 45 mmol.min; and 122 ± 54 mmol.min). When KE was given via a nasogastric tube, the initial bolus raised blood d-βHB to 2.9 ± 0.5 mM after 1 h, thereafter continuous infusion maintained blood d-βHB between 2–3 mM. Total d-βHB appearance in the blood was identical for both methods of administration (Serial drinks AUC: 1,394 ± 64 mmol.min; NG infusion AUC: 1,305 ± 143 mmol.min. p = 0.6).
It was explained to me that exogenous ketones inhibit lipolysis (breaking down of fat cells), therefore triglycerides should be expected to go down. They theorize that ketones may promote transfer of triglycerides from blood into cells, which primes the pump for fat burning, but to verify would require conducting biopsies to measure blood versus tissue.
Do I still follow a ketogenic diet? Not anymore. I was strict keto for 12 weeks – enough time to experiment and learn about it. I did enjoy parts (lots of fat!) but I don’t see it as a sustainable way of eating, nor did I benefit from it health or sports performance wise (more on this in an upcoming article). But, I was following a strict keto diet – sans carbs. I think if I were to follow a ketogenic diet AND incorporate a regular carb refeed then the results may be different.
I am confused on the diet part. I’ve tried ketogenic diets and have experienced great health benefits (I’m diatabetic), but it also helped with sleeping through the night, increased energy, appetite suppression, and balancing of hormones. However forcing myself to eat fat and eliminate God foods like fruit, and trying to keep ratios of fat to protein to carbs was really hard for me. Can supplementing with the exogenic Ketones while having a diet of Proteins, veggies, fruits, healthy fats (avacado, cocnut oil, etc) and some grains (brown rice), produce ketosis?
The effects of the two exogenous ketone drinks on acid-base balance and blood pH were disparate. In solution the ketone salt fully dissociates (giving a total of 3.2–6.4 g of inorganic cation per drink), allowing βHB− to act as a conjugate base, mildly raising blood and urine pH, as seen during salt IV infusions (Balasse and Ooms, 1968; Balasse, 1979). Urinary pH increased with the salts as the kidneys excreted the excess cations. In contrast, KE hydrolysis in the gut provides βHB− with butanediol, which subsequently underwent hepatic metabolism to form the complete keto-acid, thus briefly lowering blood pH to 7.31. Electrolyte shifts were similar for both KE and KS drinks and may have occurred due to βHB− metabolism, causing cellular potassium influx and sodium efflux (Palmer, 2015).
Ketosis supplements made in poor quality, have proven to lead to side-effects such as constipation and increased levels of cholesterol and triglycerides in men, and women may also experience amenorrhea or other disruptions to the menstrual cycle. This is why it is really important to know what combination of compounds you are consuming, particularly while you are on this very strict diet because the wrong balance can really mess with you in the long term and won't give you the high performance that you are looking for.
Every 7 days, animals were briefly fasted (4 h, water available) prior to intragastric gavage to standardize levels of blood metabolites prior to glucose and βHB measurements at baseline. Baseline (time 0) was immediately prior to gavage. Whole blood samples (10 μL) were taken from the saphenous vein for analysis of glucose and βHB levels with the commercially available glucose and ketone monitoring system Precision Xtra™ (Abbott Laboratories, Abbott Park, IL). Blood glucose and βHB were measured at 0, 0.5, 1, 4, 8, and 12 h after test substance administration, or until βHB returned to baseline levels. Food was returned to animals after blood analysis at time 0 and gavage. At baseline and week 4, whole blood samples (10 μL) were taken from the saphenous vein immediately prior to gavage (time 0) for analysis of total cholesterol, high-density lipoprotein (HDL), and triglycerides with the commercially available CardioChek™ blood lipid analyzer (Polymer Technology Systems, Inc., Indianapolis, IN). Low-density lipoprotein (LDL) cholesterol was calculated from the three measured lipid levels using the Friedewald equation: (LDL Cholesterol = Total Cholesterol - HDL - (Triglycerides/5)) [51, 52]. Animals were weighed once per week to track changes in body weight associated with hyperketonemia.
Selective attention involves focusing only on relevant information while suppressing the impulse to pay attention to irrelevant distractions. A v-shaped flock of birds are displayed. The center (target) bird points in one direction and is surrounded by birds that either match the target’s direction or do not. The task is to rapidly identify which direction the target bird is pointing.
Although decreases in FFA, TG and glucose occurred, there were no significant differences between the KE and KS drinks or with intake amount. Ingestion of ketone drinks significantly decreased overall mean plasma FFA from 0.7 to 0.4 mM, TG from 1.1 to 0.9 mM and glucose from 5.7 to 4.8 mM after 1 h (all p < 0.05). Concentrations were the same as at baseline by 4 h, with FFA at 0.6 mM, TG at 0.9 mM and glucose 5.1 mM (Figures 2A–C). There was a rise in insulin concentrations 30 min following all drinks, probably due to the small amount of carbohydrate in the sweetener (Figure (Figure2D2D).
In a nutshell… WOW! The chart above shows each of the games/categories I played, showing my prior 5-day averages compared to the day I took the ketone esters. Compared to my baselines, my scores increased across the board, with the biggest improvements in spatial orientation (+32.2%), working memory (+23.7%), quantitative reasoning (21.5%), task switching (+14.9%), and information processing (+14.9%). Below are more detailed comparisons:
Taking MCT oil (medium chain triglyceride) or coconut oil (contains 60% MCT) can help boost ketone production. This is because your body absorbs MCT very quickly as it bypasses the gallbladder and into the liver to be processed into ketone bodies. Make sure you’re getting unprocessed versions of coconut oil that is labelled as ‘organic’ or ‘extra virgin’. This, along with grass-fed butter, is what I add into my ‘bulletproof’ coffees.
Intermittent fasting will significantly help the body transition into ketosis as limiting your consumption of food for that many hours will help deplete the system of any excess glucose. It’s a shock to the system and research has shown that daily fasting can have other profound effects aside from weight control such as autophagy, lowering risks of heart disease and diabetes, as well as an improvement in cognitive function. So if you’re still wondering how to get into ketosis in 24 hours, then fasting will surely kick things into gear!
Interest in the ketogenic diet is at an all-time high, and for good reason. It’s a great way to lose body fat, gain steady energy throughout the day, increase fat-burning capacity at rest and during exercise, reduce inflammation, and improve cognitive function. Keto also has a number of promising medical applications, including seizure control, enhanced efficacy of chemotherapy, and abatement of age-related cognitive impairment.
Exercising is undoubtedly important when it comes to losing weight. An added bonus of being in a state of ketosis is the ability to improve your exercise performance, but you should also remember that entering ketosis for the first time can be a bit of a challenge for a lot of people. The body is still adjusting to such a dramatic diet change, so exercising may prove to be difficult at first. The key here is to keep going.
Beta-Hydroxybutyrate (BHB) is naturally ketone body that is produced when free fatty acids are broken down in the liver. The other two types of Ketone bodies are acetoacetate (AcAc) and acetone. Ketones provide pure energy to fuel the human brain and other tissues. The elevation in ketones in your blood have been a rapidly emerging area of research and studies are continuing to show improvements in performance, brown adipose tissue, and several other possible applications.
Background and aims: Currently there is considerable interest in ketone metabolism owing to recently reported benefits of ketosis for human health. Traditionally, ketosis has been achieved by following a high-fat, low-carbohydrate “ketogenic” diet, but adherence to such diets can be difficult. An alternative way to increase blood D-β-hydroxybutyrate (D-βHB) concentrations is ketone drinks, but the metabolic effects of exogenous ketones are relatively unknown. Here, healthy human volunteers took part in three randomized metabolic studies of drinks containing a ketone ester (KE); (R)-3-hydroxybutyl (R)-3-hydroxybutyrate, or ketone salts (KS); sodium plus potassium βHB.
Plus, take a look at this promotional video from Prüvit. It claims that “ketones make the fat melt off your body”, which is simply not true (I’ll get back to this later). It also claims that if you wanted to reach ketosis naturally, you would either need to work out 10x harder and longer or be like one of the “extreme people” who “biohack their bodies” to get into ketosis, which “can take weeks or months”. For me, this is irresponsible. A keto diet can be simple and enjoyable, but this video makes switching to a healthy, real food, keto diet sound extreme and difficult while promoting an easy way out in the form of a drink. And that’s just bad advice.
Uncontrolled diabetics may face some risks in using exogenous ketones. This is because when the body is unable to produce insulin (type I diabetics and extreme type II diabetics), it is unable to get sugar or glucose into the cells. Therefore, the body will start producing ketones. If these individuals do not use an insulin injection, they can overtime build up unsafe levels of ketones (6).
If you do the same calculations as I did above for estimating fat oxidation, you’ll see that EE in this case was approximately 13.92 kcal/min, while fat oxidation was only 67% of this, or 9.28 kcal/min, or 1.03 g/min. So, for this second effort (the test set) my body did about 5% less mechanical work, while oxidizing about 25% less of my own fat. The majority of this difference, I assume, is from the utilization of the exogenous BHB, and not glucose (again, I will address below what I think is happening with glucose levels).
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