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.
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.
The major determinant of whether the liver will produce ketone bodies is the amount of liver glycogen present (8). The primary role of liver glycogen is to maintain normal blood glucose levels. When dietary carbohydrates are removed from the diet and blood glucose falls, glucagon signals the liver to break down its glycogen stores to glucose which is released into the bloodstream. After approximately 12-16 hours, depending on activity, liver glycogen is almost completely depleted. At this time, ketogenesis increases rapidly. In fact, after liver glycogen is depleted, the availability of FFA will determine the rate of ketone production. (12)
In the second of these posts I discuss the Delta G implications of the body using ketones (specifically, beta-hydroxybutyrate, or BHB, and acetoacetate, or AcAc) for ATP generation, instead of glucose and free fatty acid (FFA). At the time I wrote that post I was particularly (read: personally) interested in the Delta G arbitrage. Stated simply, per unit of carbon, utilization of BHB offers more ATP for the same amount of oxygen consumption (as corollary, generation of the same amount of ATP requires less oxygen consumption, when compared to glucose or FFA).
If you truly want to optimize health and performance, magnesium should not be neglected. There is still more research to be done on its potential. Good sources of magnesium include whole grains, nuts, seeds, legumes, green leafy vegetables, and supplements. However, be careful about taking too much magnesium at one time, or else you might end up running to the bathroom in a hurry.
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 are three types of ketones produced when you’re on ketogenic diet: acetoacetate, beta-hydroxybutyrate (BHB), and acetone. The kinds that you’ll find in your supplements are BHB because your body can readily use and absorb them. This means that not all ketones are created equal and there are several different types, each with unique properties that are worth considering when shopping.
There are enticing anecdotes of supplemental ketones being used to boost human physical performance in competitive events, notably among elite cyclists. Given that BOHB can deliver more energy per unit of oxygen consumed than either glucose or fatty acids (Sato 1995, Cox 2016, Murray 2016), this makes sense. But what we do not know is if there is any required period of adaptation to the use of exogenous ketones, and thus how to employ them in training. It is clear that exogenous ketones decrease adipose tissue lipolysis and availability of fatty acids, the exact opposite to what happens on a well formulated ketogenic diet. This distinction between exogenous ketones and ketogenic diets on adipose tissue physiology and human energy balance underscores an important reason why these two ketone-boosting strategies should not be conflated.
Long-Term Effects of a Ketogenic Diet in Obese Patients – The present study shows the beneficial effects of a long-term ketogenic diet. It significantly 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.(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2716748/)
Intense exercise -- more than just fidgeting or pacing -- uses ketones, when glucose is in short supply, which means the body has to create more ketones to replace what you use. This is great for those who are used to a moderate to intense activity level, but intensity is a fine dance between encouraging ketone production and elevating cortisol for the rest of us.
However, it's important to NEVER overlook the power of exercise and of course sticking to a proper routine to get the most optimized results. The most common mistake people make is by treating any keto supplement like a "wonder drug" that will help them shred weight in their sleep. Seriously... how is that even scientifically possible. So if you are thinking about trying out a particular supplement, I would suggest two things:
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).
We designed a test for each of the chosen benefit claims and enlisted the help of four of our Diet Doctor teammates to try out the supplements and go through the testing. They were Jonatan and Giorgos from the video team, Emőke from the recipe team and Erik from the IT team. We had a mix of people who were naturally in endogenous ketosis during testing, and people who were not.
Testing BHB levels in the blood is simple but can get pricey if you are doing it many times a day. The Precision Xtra blood glucose and ketone meter is a good buy at $28-$30. The expensive part is the ketone test strips here which can cost $4 each. If you are looking at testing yourself every day it is going to cost you $120 a month and the $30 meter. Here is a starter kit you can get on Amazon.
I feel like I should also mention that the GI discomfort is real, people. I would recommend starting this product on a weekend or a day where you’re able to just take it easy. After my first dose, which was only 1/2 scoop, I literally just felt like lying in bed all day due to feelings of nauseousness; however, by the next day I was fine and even bumped my dose to a full scoop.
The table below shows the same measurements and calculations as the above table, but under the test conditions. You’ll note that BHB is higher at the start and falls more rapidly, as does glucose (for reasons I’ll explain below). HR data are almost identical to the control test, but VO2 and VCO2 are both lower. RQ, however, is slightly higher, implying that the reduction in oxygen consumption was greater than the reduction in carbon dioxide production.
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