June 12, 2018


My experience with exogenous ketones

Theory to anecdote: I decided to find out for myself if ketones could, indeed, offer up the same amount of usable energy with less oxygen consumption.

Read Time 10 minutes

I wrote this post at about the same time Germany won the World Cup in Rio de Janeiro in 2014. There’s been a lot of moving and shaking in the world of exogenous ketones since then, not to mention soccer. Looking back on my post, I still consider it relevant in terms of what exogenous ketones possibly can (and cannot) do for performance. In this case, to see if exogenous ketone esters provide me a “boost” by allowing me to do the same amount of work while expending less energy (and work at a relatively lower VO2) compared to no supplementation.

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?

Caveat emptor: the following post doesn’t come close to answering most of these questions. I only document my experience with BHB salts (and a non-commercial version at that), but say little to nothing about my experience with BHB esters or AcAc esters. But it will provide you will some context and understanding about what exogenous ketones are, and what they might do for athletic performance. We’ll likely podcast about the questions and topics above and cover other aspects of exogenous ketones in more detail.

—P.A., June 2018


Original publication date: August 14, 2014

Last year I wrote a couple of posts on the nuances and complexities of ketosis, with an emphasis on nutritional ketosis (but some discussion of other states of ketosis—starvation ketosis and diabetic ketoacidosis, or DKA). To understand this post, you’ll want to at least be familiar with the ideas in those posts, which can be found here and here.

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).

I also concluded that post by discussing the possibility of testing this (theoretical) idea in a real person, with the help of exogenous (i.e., synthetic) ketones. I have seen this effect in (unpublished) data in world class athletes not on a ketogenic diet who have supplemented with exogenous ketones (more on that, below). Case after case showed a small, but significant increase in sub-threshold performance (as an example, efforts longer than about 4 minutes all-out).

So I decided to find out for myself if ketones could, indeed, offer up the same amount of usable energy with less oxygen consumption. Some housekeeping issues before getting into it.

  1. This is a self-experiment, not real “data”—“N of 1” stuff is suggestive, but it prevents the use of nifty little things likes error bars and p-values. Please don’t over interpret these results. My reason for sharing this is to spark a discussion and hope that a more systematic and rigorous approach can be undertaken.
  2. All of the data I’ll present below were from an experiment I did with the help of Dominic D’Agostino and Pat Jak (who did the indirect calorimetry) in the summer of 2013. (I wrote this up immediately, but I’ve only got around to blogging about it now.) Dom is, far and away, the most knowledgeable person on the topic of exogenous ketones. Others have been at it longer, but none have the vast experiences with all possible modalities (i.e., esters versus salts, BHB versus AcAc) and the concurrent understanding of how nutritional ketosis works. If people call me keto-man (some do, as silly as it sounds), they should call Dom keto-king.
  3. 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.
  4. The ketone esters are, hands-down, the worst tasting compounds I have ever put in my body. The world’s worst scotch tastes like spring water compared to these things. The first time I tried 50 mL of BHB monoester, I failed to mix it with anything (Dom warned me, but I was too eager to try them to actually read his instructions). Strategic error. It tasted as I imagine jet fuel would taste. I thought I was going to go blind. I didn’t stop gagging for 10 minutes. (I did this before an early morning bike ride, and I was gagging so loudly in the kitchen that I woke up my wife, who was still sleeping in our bedroom.) The taste of the AcAc di-ester is at least masked by the fact that Dom was able to put it into capsules. But they are still categorically horrible. The salts are definitely better, but despite experimenting with them for months, I was unable to consistently ingest them without experiencing GI side-effects; often I was fine, but enough times I was not, which left me concluding that I still needed to work out the kinks. From my discussions with others using the BHB salts, it seems I have a particularly sensitive GI system.

The hypothesis we sought out to test

A keto-adapted subject (who may already benefit from some Delta G arbitrage) will, under fixed work load, require less oxygen when ingesting exogenous ketones than when not.

Posed as a question: At a given rate of mechanical work, would the addition of exogenous ketones reduce a subject’s oxygen consumption?

The “experiment”

  • A keto-adapted subject (me) completed two 20-minute test rides at approximately 60% of VO2 max on a load generator (CompuTrainer); such a device allows one to “fix” the work requirement by fixing the power demand to pedal the bike
  • This fixed load was chosen to be 180 watts which resulted in approximately 3 L/min of VO2—minute ventilation of oxygen (this was an aerobic effort at a power output of approximately 60% of functional threshold power, FTP, which also corresponded to a minute ventilation of approximately 60% of VO2 max)
  • Test set #1—done under conditions of mild nutritional ketosis, while still fasted
  • Test set #2—60 minutes following ingestion of 15.6 g BHB mineral salt to produce instant “artificial ketosis,” which took place immediately following Test set #1
  • Measurements taken included whole blood glucose and BHB (every 5 minutes); VO2 and VCO2 (every 15 seconds); HR (continuous); RQ is calculated as the ratio of VO2 and VCO2. In the video of this post I explain what VO2, VCO2, and RQ tell us about energy expenditure and substrate use—very quickly, RQ typically varies between about 0.7 and 1.0—the closer RQ is to 0.7, the more fat is being oxidized; the reverse is true as RQ approaches 1.0


Test set #1 (control—mild nutritional ketosis)

The table below shows the data collected over the first 20 minute effort. The 20 minute effort was continuous, but for the purpose of presenting the data, I’ve shown the segmental values—end of segment for glucose and BHB; segment average for HR, minute ventilation (in mL per min), and RQ; and segment total for minute ventilation (in liters).

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.

The graph, below, shows the continuous data for VO2, VCO2 (measured), and RQ (calculated).

Test set #2 (ingestion of 15.6 g BHB salt 60 minutes prior)

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.

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).

The graph once again shows the continuous data for VO2, VCO2 (measured), and RQ (calculated).

Side-by-side difference

The final graph, below, shows the continuous data for only VO2 side-by-side for the 20 minute period. The upper (blue) line represents oxygen consumption under control conditions, while the lower line (red) represents oxygen consumption following the BHB ingestion. In theory, given that the same load was being overcome, and the same amount of mechanical work was being done, these lines should be identical.

The hypothesis being tested in this “experiment” is that they would not be the same. Beyond visual inspection, the difference between the lines appears to grow as the test goes on, which is captured in the tabular data showing 5 minute segmental data.


The most obvious limitation of this endeavor is the fact that it’s not an appropriately controlled experiment. Putting that aside, I want to focus on the nuanced limitations—which don’t impact the primary outcome of oxygen consumption—even if one were appropriately doing a real experiment.

  1. It’s not clear that the Weir coefficients used to estimate EE are relevant for someone in ketosis, let alone someone ingesting exogenous BHB. (The Weir formula states that EE is approximated by 3.94 * VO2 + 1.11 * VCO2, where VO2 and VCO2 are measured in L/min; 3.94 and 1.11 are the Weir coefficients, and they are derived by tabulating the stoichiometry of lipid synthesis and oxidation of fat and glucose and calculating the amount of oxygen consumed and carbon dioxide generated.) While this doesn’t impact the main observation—less oxygen was consumed with higher ketones—it does impact the estimation of EE and substrate use.
  2. 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.”

Observations from this “experiment” (and my experience, in general)

Animal models (e.g., using rat hearts) and unpublished case reports in elite athletes suggest supplemented BHB produces more ATP per unit carbon and per unit oxygen consumed than glycogen and FFA. This appears to have been the case in my anecdotal exercise.

The energy necessary to perform the mechanical work did not appear to change much between tests, though the amount of oxygen utilization and fat oxidation did go down measurably. The latter finding is not surprising since the body was not sitting on an abundant and available source of BHB—there was less need to make BHB “the old fashioned way.”

As seen in this exercise, glucose tends to fall quite precipitously following exogenous ketone ingestions. Without exception, every time I ingested these compounds (which I’ve probably done a total of 25 to 30 times), my glucose would fall, sometimes as low as 3 mM (just below 60 mg/dL). Despite this, I never felt symptomatic from hypoglycemia. Richard Veech (NIH) one of the pioneers of exogenous ketones, has suggested this phenomenon is the result of the ketones activating pyruvate dehydogenase (PDH), which enhances insulin-mediated glucose uptake. (At some point I will also write a post on Alzheimer’s disease, which almost always involves sluggish PDH activity —in animal models acute bolus of insulin transiently improves symptoms and administration of exogenous ketones does the same, even without glucose.)

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.

If that explains the hypoglycemia, it would seem the absence of symptoms can be explained by the work of George Cahill (back in the day; see bottom figure in this post)—when ketone levels are high enough they can dominate brain fuel, even ahead of glucose.

Finally, these compounds seemed to have a profound impact on my appetite (they produced a strong tendency towards appetite suppression). I think there are at least two good explanations for this, which I plan to write about in a dedicated post. This particular topic—appetite regulation—is too interesting to warrant anything less.

Open questions to be tested in real experiments

  1. Are these results reproducible? If so, how variable are the results across individuals (by baseline metabolic state, diet, fitness)?
  2. Would the difference in oxygen consumption be larger (or smaller) in an athlete not already keto-adapted (i.e., not producing endogenous ketones)?
  3. Would the observed effect be greater at higher plasma levels of BHB (e.g., 5 to 7 mM), which is “easily” achievable with exogenous ketones?
  4. Would the observed effect be the same or different at higher levels of ATP demand (e.g., at FTP or at 85-95% of VO2 max)?
  5. Would the trend towards improved energy efficiency continue if the exercise bout was longer in duration (say, greater than 2 hours)?
  6. How will exogenous ketones impact exercise duration and lactate buffering?
  7. Why do exogenous ketones (both BHB and AcAc it seems) reduce blood glucose levels so much, and can this feature be exploited to treat type 2 diabetes?
  8. Are there deleterious effects from using exogenous ketones, besides GI side-effects?
  9. What are the differences between exogenous BHB and AcAc (which in vivo exist in a reversible equilibrium) on this particular phenomenon? (Work by Dom D’Agostino’s group and others have shown other differences in metabolic response and clinical application, including their relative impact on neurons.)

Photo by Alexey Lin on Unsplash

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  1. I’m sure I don’t know how to tease apart the acute and chronic effects of fasting, or CHO restriction, from the overlapping acute and chronic effects of moderately elevated ketone bodies in circulation. Have always thought of ketosis and CHO restriction together, with good reason as they have generally occurred together – until this advent of ketone precursors. Now the state of moderate ketosis, with no particular dietary restriction necessary, I don’t think we’ve seen that before. I appreciate the n=1 work, please continue as you can, and I really hope there can soon be more formal exploration of what is possible with ketone precursors. MCTs are useful but these ester ketone precursors appear to hold much potential to show what new metabolic possibilities may exist.

    In my work, I sometimes have compelling reasons to prescribe medications that, although they may be necessary, proceed to induce the metabolic syndrome in the patients. And of course this adverse metabolic condition has been increasing in incidence, overall. So in addition to exercise effects, I’m interested in possible ketone precursor benefits for metabolic syndrome, or of course for Type II DM.

    Induced ketosis may offer chronicaly lowered glucose and insulin levels, decreased appetite through increased brain malonyl CoA or other mechanisms, increased mitochondrial biogenesis, and through effects on the carbohydrate response-element binding protein mobilization, may further tip hepatic cell metabolism away from lipogenesis and toward lipolysis and beta-oxidation. So, could be good for fatty liver disease and related metabolic problems.

    I think CHO restriction is a dietary change that individuals at risk for the metabolic syndrome and its related illnesses should make. But I’ve been wondering if the acute change in appetite and metabolism provoked by ketone precursors could serve as a helpful bridge to beneficial dietary change in individuals who otherwise might not change their dietary patterns due to habit or food cravings.

    It would be expensive and months-long (to be done well) but I hope we can one day see a trial of diet and exercise lifestyle intervention in patients with metabolic syndrome or DM II, with double-blind rating and randomized assignment to a ketone precursor or a (suitably nasty tasting) placebo. Compliance with the study agent should not be difficult to objectively determine – measure ketones along with the other variables. Outcome measures BMI, waist circumference, A1C, diastolic BP, HDL, etc – maybe CRP and IL1, IL6 too.

    Please keep us informed on this area. If you were to pick a ketone precursor to trial as above – do you have an opinion yet which one would be practical to ingest?

    Rob Coberly

    • Yes, I think malonyl CoA is one of the mechanisms by which exogenous ketones reduce appetite. I also think the liver “sees” more ATP and that message gets to the brain.
      Not sure the answer to your question, though. From a regulatory standpoint the BHB salts are going to hit the market first (before BHB esters and AcAc esters), I suspect, since they already have GRAS approval.

  2. Thanks. I only came across the concept recently, and I wondered what you thought about it. Who else would be worth looking into? I am pretty much untrained as of now, though not historically. Should I get right to it or start with something more “traditional”?

    Sorry for going off topic.

  3. I think much light is shed into this as long as you put it in an evolutionary perspective. I also think that this could be reproducible over longer durations as long as you keep providing exogenous ketones or as long as your body has enough bodyfat to sustain ketogenesis. Yet, tests need to be done!

    Great quantified experiment Doc 😉

  4. Informative post!
    I had a question when you stated…

    The latter finding is not surprising since the body was not sitting on an abundant and available source of BHB—there was less need to make BHB “the old fashioned way.”

    With exogenous ketones wouldn’t there be an abundant available of BHB?

  5. This is really interesting. I can see the enormous potential for exogenous ketones to help with weight loss, and metabolic syndrome, but their potential effect on athletic performance and stamina has intrigued me. The fact that these ketones increase oxygen efficiency blows my mind. I immediately thought of the benefits for high altitude mountaineering like a previous poster, but it looks like they might work to bump someone in nutritional ketosis into a temporary metabolic state of super efficiency fueled almost entirely by ketones, so any endurance athlete in NK would improve performance by ingesting exogenous ketones immediately prior to exercise. I wonder about the mechanism for this oxygen efficiency? Really interesting stuff.

    It also made me wonder if it might help folks with COPD?

    Thanks very much for this. Fascinating and I will bet many athletes will take notice if they have not already. Do you know the timetable for when we might see the BHB salts hit the market?

    • Yes, assuming they can be made to taste ok and are found to not be harmful with long term use, there are many applications, as you suggest.

  6. I think ketosis is an emergency mode our bodies go into to remove all of the excess fat we have accumulated as a result of eating all of the sugar and carbohydrates in our modern day diet. Our bodies want to be lean and mean in order to prosper and breed and care for our young properly. Fight and flight. Fat we can’t do that effectively.

    • Hmm…personally, I think it’s more the natural metabolic state of human beings. If you imagine a scenario 50,000 years ago (or 200,000 or 1 million), abundance of dietary carbohydrates probably was the equivalent of no animal food source, and potentially starvation was on the way.

      This corroborates nicely with the insulin/enzyme/fat storage thought process, because lots of insulin promotes fat accumulation, which is what humans ought to be doing if they are lacking decent sustenance.

      Obviously, this oversimplifies it, because humans have always been opportunistic omnivores (early H. Erectus was probably a scavenger). Geography would have played an important role, as well, which is why fish was such a major dietary staple for so many Africans and Europeans for so long. It stands to reason that many of our biological adaptations would have gone hand-in-hand with high fish consumption

  7. Dr. Attia — thanks for such an interesting post. I always look forward to reading your latest post. You certainly sound like a busy guy, so I wanted to thank you for taking the time out of your schedule to put this information out there. I’ve learned so much from reading your posts over the years that I wanted to finally thank you; it has absolutely made me contemplate how I live my life.

  8. Hi Peter,
    Thanks for all that you share with us.
    Just wondering if could help clear up some confusion for me. It was my understanding that after keto-adaptation, muscles primarily use free fatty acids as fuel and spare ketones for use by the brain. Is this accurate?
    If it is then you might get what I’m trying to understand here. If ketones are spared for the brain and muscles primarily use FFA as fuel after keto adaptation, then why would ketone supplementation help physical performance?

    • Not necessarily. Muscles also use ketones–perhaps some more than others (e.g., heart probably uses more than skeletal; not sure about smooth).

  9. I agree that appetite regulation is an important topic. Experienced myself that just after one week low-carb I had less appetite. This in itself might be a reason why low-carb is so successful. I guess it is natural for the body to indicate that ‘you are doing fine, no need to eat’, but this needs to be scientifically proven, ie as mentioned in one of your video talks a good cocaine addiction also makes you less hungry and lose wait.

  10. Hi Peter,

    Since ketones are generated from the breakdown of fatty acids, it makes sense that there is a linear relationship between BHB levels and fatty acid oxidation. Have you found this to be the case empirically?

    Thanks, Aaron

  11. thanks for the detailed post peter. we are getting ready to introduce a powdered bhb salt (calcium and sodium combo) that is flavored, pH adjusted, and quite palatable. just mix with water.

  12. Hi Peter, fantastic article! Can I help you answer some of the open questions? I recently quit my day job as a software engineer at a hedge fund to start a new practice with a medical doctor. We’re both elite level mountain bikers. Ketosis has improved my life in ways I never could have anticipated and I’m really keen to further the research. I met Dominic at AHS and will be interviewing him for our podcast in couple of weeks, can you put me in touch with anyone in California with the equipment and knowhow?

  13. Have you come across a decently accurate way of measuring an individuals insulin response to artificial sweeteners since this is being talked about as a possibility? I keep wondering if C peptide could be used for this or if an actual immunoassay would be required, or if you could even get an actionable number from an antecubital blood draw for something like this. If you try and ascertain this with diet and a glucose/ketone meter it just seems like it would (or could) potentially take a while (days or weeks) to get anywhere near an accurate picture of one’s response.
    I am definitely going to try some of Patrick A’s BHB salts. Have you tried chilling any of the esters as cold as possible before consuming them? That might help although from what you describe it sounds like it might take a miracle flavoring agent to get them gag proof and I drink Laphroaig from time to time, which to me always seems to have this quality of a Betadine soaked bandage to it, but that’s just me 🙂

    I may have to look up Dom one day as I am always over at Moffitt or M2Gen working on a robot or 2 of theirs.

    As always a big thanks for your efforts and time.

    It is much appreciated!


    • Better tasting agents are on the way. I think the AcAc di-ester and the BHB salts are the way forward. I see no advantage to the BHB mono-ester.
      To your first question, I’d suck it up and do the RIA to find out for sure.

  14. Yeah. I just hate to add to the RIA workload of some poor bench tech out there although I suppose in this day and time they may have a fluorescence based version of the assay. I know what a huge PIA radioimmunoassay’s can be. When I first got out of university I got a bench tech job working for LabCorp’s Center for Molecular Biology and Pathology doing an RIA for unconjugated estriol in the Biochemical Genetics Lab. They used the Foundation for Blood Research’s algorithm for risk screening for pregnancies for Trisomy 18, 21 and open neural tube defects. Ue3 was a critical analyte for the algorithm. Our assay used I-123 and I did anywhere from 700 to 1000 patient samples every evening. Using giant centrifuges with these custom rotors to spin down huge racks of vials. Dealing with (potentially) radioactive water baths and this huge ancient automated scintillation counter that was always getting jammed. Then we had to hand transcribe all the results. Eventually I ended up performing radioactive PCR for Fragile X Syndrome in the Molecular Genetics/Molecular Oncology/Pharmacogenomics department before I matriculated into lab management although I was still radiation safety officer even when I was managing the lab. Used to log in 32P and 35S Methionine every week and dealt with all the decay and disposal. So after all that I just have this aversion to radioactive anything with an aversion to lab management in close second place. Now I I’m just a lab automation jock for Qiagen driving all around my good ‘ol home state of Florida trying to find a way out of this NIDDM maze I have gotten myself into. You and many of your colleagues have been a tremendous help with showing me the way when most of the health care professionals I have been to just want to pump me full of what I consider to be subpar options on the good end and just outright dangerous on the bad end, like Byetta. I only have 1 kidney because of an undiscovered elongated left ureter that kinked up and caused primary hydronephrosis that had destroyed the kidney on that side by the time the repair was initiated. The removal had to be done through the vertical incision (lumbotomy?) through which the repair of the ureter was supposed to be facilitated. As a surgeon I’m sure you can imagine how these guys ended up getting through that. Took forever from what I was told. Anyway, I want to try a low dose of Metformin but there is always this looming lactic acidosis issue so I need to find somebody that is willing to work with me although the last time I saw my nephrologist he said I had the highest eGFR he had ever seen especially for someone with one kidney. He was walking around showing the result to all of his residents over at USF. I am also wondering if I can get some decent suppression of liver GNG, possibly on par with Metformin, from the BHB salts. Only one way to find out I guess. On with my N of 1. We should all get T-shirts made or something 🙂

    Thanks again for all the inspiration!

  15. Dr Attia

    Phenomenal post as usual. The slow drip of information that your blog provides is worth its weight in gold. I’m currently in ketosis and plan on utilizing the body by science routine. I was initially thinking of taking something like ucan before my exercises in order to prevent bonking. I realize this is preliminary, but do you think exogenous ketones can be used in place of ucan to prevent bonking.

  16. Peter, your nearly-obsessive level of detail and experimentation is what makes eating academy unique. I devour every article and I thank you for making me smarter.

    You made me change my diet (along with Taubes), and I really hope your studies results at NuSi change the world of nutrition forever.

    Now that I’m done inflating your ego, I wanted to know if you heard about KetoForce. It’s a product made up of BHB salts http://prototypenutrition.com/ketoforce.html so in theory it would work exactly like the esters, no?

    My only worry is that excess exogenous ketones could cause acidosis, and hypoglicemic shock…since the body stops ketone production by secreting insulin, maybe taking too many ketones can do that when the body secretes more insulin to maintain equilibrium, perhaps sugar would be beneficial to at least maintain blood glucose?

    How much is too much when taking exogenous ketones?

    • Yes, ketoforce is a BHB salt prep (I don’t recall which salt this is). In theory they should work like the ester, but I’m not sure that is entirely the case. They certainly taste better.
      I’m sure one can take too much, but I don’t think such levels have been established.

  17. Dr. Attia,

    Thank you for what you do. I have sort of awoken to my dire situation and have found your blog helpful. My numbers from 2 weeks ago are horrible:
    LDL-P number 1900
    Small LDL-P 1600
    HDL-C 32
    LDL-C 110

    From what I have read, I am a ticking time bomb. Argh it sucks. I have a very young daughter and I am only 34 (6.1″ and 195 pounds). I am trying to now go on the no carb kind of diet but just worry if it is too late.
    Btw, I live in San Diego. But I think you do not actively practice since I could not find your information anywhere. I will probably go see Dr. Triffon.

    • Those LDL-P are not as terrible as you think. But plenty of room to improve.

      Study fatty acid compositions and you will see that there are four specific types of saturated fat, and different foods have these in different compositions. What I found by experiment is that my N=1 is that only certain types of saturated fat elevate my LDL-P. For some reason dairy cream makes my LDL explode. I went up to LDL-P of 2300. To contrast, coconut milk, animal fat, and moderate indian ghee I seem to tolerate. Just by excluding the dairy fats in cream I got my LDL-P to 1600 and it is still coming down. Once you understand relative fatty acid compositions of the fats you eat, you can start to do targeted experiments and repeat the NMR lipoprofile periodically to see which fats most affect your numbers either way.

  18. Don’t know how these work, but it seems like the rate of available ATP could be higher and last longer than ketones, aerobic, anaerobic, phosphorus. If true it could help in everything from reaction times to burst events/sports? Which would bring into being a whole new modality of training. Seriously? Say it ain’t true!

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