Back in 1995 Veech was looking at a ketone mixture as physiologically equivalent to insulin/glucose. In order to limit his variables the isolated rat myocardia used in the study were perfused with Krebs-Henseleit buffer containing the metabolic milieu of interest. The buffer has no free fatty acids so takes the provision of acetyl CoA from beta oxidation right out of the equation. It also eliminates any uncoupling from free fatty acids in the perfusate. It took me a while to twig that this was potentially a very long way from the situation under fasting or ketogenic diet conditions where free fatty acids might well be at the maximal physiological levels whenever ketones hit 5.0mmol/l.
The idea was certainly in mind when the group published this, in 2004:
“Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins. New diets comprised of ketone bodies themselves or their esters may obviate this present difficulty.”
By 2012 the problem with ketogenic diets had been reduced to one of impossible compliance, rather than metabolic inefficiency of free fatty acid metabolism:
"Further, to achieve effective ketosis with KG diets, almost complete avoidance of carbohydrates is required to keep blood insulin levels low to maintain adipose tissue lipolysis. Such high-fat, no-carbohydrate diets are unpalatable, leading to poor patient compliance."
You notice the uncoupling, previously a potential problem, is now in the title of the paper. Ketones in real life, even from ketone esters, work in a milieu of free fatty acids. If you flood the mitochondria with ATP-generating ketones, which generate no ATP in the cytoplasm, you just might expect to open that uncoupling pore and allow a few FFAs to translocate some protons, to limit over production of ATP within the mitochondria.
Currently, in 2014, the delectable savour-the-flavour of ketone esters allows this:
“…the ester can be taken as an oral supplement without changing the habitual diet.”
I watch this stuff with some degree of amazement. There is a suspicion that AD incidence is increasing rather faster than an ageing population would explain. The suggestion is that it has an environmental component. Now, many potential explanations are possible but I would like to think it is the saturophobic, cholesterophobic, fructophilic low fat based dietary advice from the American Heart Association which is the prime driver. Seems likely.
If AD (also known as type 3 diabetes) is a dietary disease, much as type 2 diabetes is largely a dietary disease, providing a crutch which will allow you to cling to the diet which got you in to AD in the first place strikes me as the biggest risk from ketone esters.
Excepting the stale urine/sweaty socks yummy aroma of course. Bring on the egg yolks fried in butter as an alternative, please.
A ketogenic diet features several things in addition to ketones. There is the chronic normoglycaemia which is anathema to the Crabtree effect. There is the physiological rock bottom basement insulin levels in a system where insulin signalling is f*cked. There are the elevated free fatty acids. These are the best.
Those free fatty acids are taken up by astroglial cells and used to generate in-situ ketone bodies. What sort of levels do they supply in vivo? That's an unknown (as far as I can tell), but I'm willing to bet that FFA supply under true ketogenic eating is both high and consistent, irrespective of fed/fasted state.
This is not quite the case if you are on the old MCT kick or mainlining sweaty socks while munching crapinabag.
A little background about Dr and Mr Newport and ketones which triggered this post off:
I have been unable to tease out, from Dr Newport's original article, that of Emily Deans or from the abstract of the case report above, quite what level of carbohydrate Mr Newport consumed in the original MCT phase, during the drug trial or while on ketone esters. I suspect it might have been more than a banana a day.
Oh, and another addendum. I, personally, clearly have issues with faking a ketogenic diet. This is true. But let me not decry ketones or their esters per se. If MCT oil or ketone esters get you out of bed and let you get dressed without needing assistance, that's great. They sure as hell knock spots off of anything which Big Pharma has to offer for AD management. The fact that I have yet to die as a direct result of eating less than one banana a day means that I hope never to need ketone esters. I feel a ketogenic diet should be high on the agenda for those with neurodegenerative diseases, with ketone esters or MCTs as a fall back. But then I would, wouldn't I...
Tuesday, October 28, 2014
Are ketone esters dangerous?
Posted by Peter at Tuesday, October 28, 2014
Labels: Are ketone esters dangerous?
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"Such high-fat, no-carbohydrate diets are unpalatable, leading to poor patient compliance."
I'd like to invite him over to dinner at my house. My wife and I refer to this as the "Cheating Diet", since you get to eat all the stuff you've traditionally been told not to eat. :)
I agree. A KD is "just the good stuff." How it can be enhanced by adding starch or sugar, I don't know.
The amount of carbs in the case report isn't stated, although definitely not ketogenic: 1) it says he adhered to his "normal" diet; and 2) the ketones were mixed in "soda-flavored syrup," and he was ingesting a LOT of ketones... almost 90 grams daily! Here's a link to the full text: http://bit.ly/1rS7Dny.
That said, his recovery was immediate and amazing.
"I feel a ketogenic diet should be high on the agenda for those with neurodegenerative diseases..." I find it interesting that you can also hear/read this opinion from some of those that otherwise promote carbohydrates as being vital/essential.
If a dementia sufferer's brain prefers ketones (or lactate?) over glucose, is there are a simple, logical reason why a healthy brain wouldn't?
That's not a rhetorical question, I'm honestly curious given that there appear to be some very strong opinions on long-term ketosis being dangerous or at least not ideal.
If it comes down to an individual's ability to metabolise glucose for brain food, then it seems a risky bet to simply assume that your particular brain is quite OK with that.
Thanks Bill, nice to get a few more bits in to place.
Spittin’, opinion is opinion. It’s like clinical experience, a particularly poor guide to efficacy. I keep thinking of the poor chap who was so very anti ketogenic eating because it induces autophagy. Autophagy was considered to be Bad, based on an easily destructable paper. He was avoiding utilising this cell repair system. I guess he likes sugar.
Given a fully functional PDH complex, do ketones have any benefit over lactate is the question. That’s a deeply important question. The answer is possibly not, but only IF you have a fully functional PDH complex. So if we are going to use lactate combined with insulin signalling we should be OK, so long as we are OK. Unfortunately I’m getting older and the chances of my being normoglycaemic on a mixed diet get lower with the passing of the years. I’m looking to avoid the Crabtree effect and the easiest way appears to be low grade ketosis. I need hard core evidence that ketosis is bad before I abandon it for the alternative of intermittent hyperglycaemia…
And that's ignoring all the probable actively beneficial effects of chronically low insulin levels.
Great blog entry Peter.
I agree using ketone salts vs following the ketogenic diet for a neurological condition is sort of like drinking a glass of water when you are poisoned vs taking activated charcoal/stomach pump. It helps more than doing nothing at all, but compared to real keto diet it's a joke.
" I'm willing to bet that FFA supply under true ketogenic eating is both high and consistent, irrespective of fed/fasted state."
I'm willing to bet this too ;)
FFAs are the real mechanism of action of keto diet for excitatory mental conditions such as seizures , likely MI as well, a proper ketogenic diet is required to benefit. OTOH, ketone esters are glucose-like, suppress FFAs and evoke insulin. For a dementing totally IR alzheimers patient perhaps this might be useful to supply alternative energy source as well as increase central insulin expression via ketone salts (insulin has been shown to help dementia, ironically the insulin tropic nature of ketone salts may help alzheimers). All the same I'm pretty darn sure a real keto diet is way waaay better than crap ketone esters.
For seizures (and likely MI where benefit of keto is superior glutamate processing/Ca&Na block/reduced excitatory tone ) taking ketone salts does jack crap. OTOH the FFAs portion of the keto diet block the Ca/Na channels and this is dose dependent (that is raising FFAs makes the keto diet work better).
It's shown over and over: no correlation between ketone #s and seizure control, however BIG correlation between keto diet compliance and control. I see no reason why alzheimers would be that much different, another excitatory hypometabolic CNS disease.
All neuro patients pretty much stand to benefit from UCP mitochondrial biogenesis which is another FFA dependent function that ketone ester/salts actively insult.
It is really tragic this "magic ketone" red herring is drawing attention away from the REAL MECHANISM OF ACTION of ketogenic diets, which is the lower glucose/higher FFA milieu. Ketones vs a ketogenic diet is as stated, a near useless intervention relative to a possibly curative, life saving one.
So you drink 60 measly calories of ketone salts and wow your ketone meter says 4. Big deal. Guess what, if I consumed 2000 calories of an 80% fat diet, that is a LOT, LOT more ketones in my brain over the day, isn't it now?
Maybe my meter only says "0.5-1.4" of excess ketones in my blood, but bet your bottom dollar net ketones are WAAAY higher 24 hrs a day in my CNS while on a modified atkins diet. Drinking a shot of ketones 4 times a day is a joke in comparison.
I want to repeat: I don't think people realize just how little energy ketone esters actually are. 1 serving is 60 calories. That is not going to fuel or save a dementing brain. Furthermore this number is at a cost of ketone salt induced insulin secretion to lower FFA and increase glucose oxidation in the body. At the site of the brain FFA transport depression via ketone ester insulintropic stimulus, maybe you break even steven. More ketones coming in, but less FFAs (which are ketogenic in CNA). Almost a wash.
" If MCT oil or ketone esters get you out of bed and let you get dressed without needing assistance, that's great. They sure as hell knock spots off of anything which Big Pharma has to offer for AD management.
I feel a ketogenic diet should be high on the agenda for those with neurodegenerative diseases, with ketone esters or MCTs as a fall back. But then I would, wouldn't I... "
The paper (I have the full text) does not list the carbohydrate content of the Newport diet. I think ketone esters would be useful to establish which patients would benefit from ketogenic diets, then you could differentiate up front, as it often takes a few months to really kick in, and if ice cream is the only joy in grandpa's life, he needs good reason to give it up. I would be surprised if the original Newport diet had more than 70g of carbs daily even with the MCT oil considering the levels of ketosis reportedly maintained. But I'm just guessing.
I came across a few (very few) studies where they fed non-esterified fatty acids (NEFAs) to animals on a zero-carb diet. The animals ended up with very low insulin and glucose levels (and they didn't grow well).
I wondered why they had never tested it on humans. Now I know. I made NEFAs at home, first from canola oil, then from coconut oil. It tastes bad. It smells worse. It is very irritating (mouth, throat, nose), especially the coconut. NOT NICE.
It does, however, improve my hypertension.
Now I wonder how the original researcher could simply omit the fact that the chow must have tasted/smelled/felt awful to the lab animals, leading them to starve, and explaining the low glucose and insulin (and poor growth). Weirder still, they reported that adding some carbs to the diet reversed the effects of the NEFAs. I cannot imagine at all how adding a few grams of carbs could make that thing palatable. No way.
I guess NEFAs might be useful for people with gastric tubes, though. Has anyone seen any study where they feed NEFAs to humans?
There are many opportunities to re-create foods like an ice-cream in a LC form, but I guess it is viewed as too much trouble by the majority of our population. OMG, if I could eat all LC deserts without gaining weight, I would be making an ice-cream which is 100% better than everything in a store all the time.
When a tragedy like an Alzheimer strikes, family members often feel hopeless and demoralized by own inability to do something except giving the sick family member some supplements and re-arrange environment into safer way, and prepare to watch the decline. I guess many would agree to organize potentially beneficial way of eating without rubbing grandpa from his last joy. Still most people think that medications are powerful while diet changes are something minor what is addressed mostly when there is no suitable bona fide medications to be recommended. Normal average people just have no idea how powerfully the choice of food may influence a mental health.
Peter -- THANK YOU for this post!
This is really the crux of things for me: "If AD (also known as type 3 diabetes) is a dietary disease, much as type 2 diabetes is largely a dietary disease, providing a crutch which will allow you to cling to the diet which got you in to AD in the first place strikes me as the biggest risk from ketone esters." Abso-friggin'-lutley!
I wrote my graduate thesis on the the potential use of LC/ketogenic diets as therapy for Alzheimer's disease. A pared down version of it was published in the summer 2014 issue of the Weston A. Price Foundation's journal. I am trying to get the word out as much as possible: http://www.westonaprice.org/modern-diseases/type-3-diabetes-metabolic-causes-of-alzheimers-disease/
I'm happy to provide a slightly more scientific version to anyone who's interested. (It contains just a little bit more of the biochemical mechanisms involved.) Feel free to email me at: tuitnutrition (at) gmail (dot) com.
Anyway, one of the lines in my paper referred the to the use of exogenous ketones/MCT oils, and how that might be helpful in the short-term, as a kind of "brain boost," but would do nothing to actually correct the underlying problem (namely, the brain's inability to properly metabolize glucose) - "In the absence of dramatic dietary overhaul, the administration of KBs is akin to bailing water out of a leaky boat without stopping to patch the hole: you merely manage the effects while the root cause continues wreaking havoc."
Just like any pharmaceutical drug -- it seems like the use of exogenous ketones is a short-term "band-aid," rather than an actual *solution* to the problem.
I didn't read paper, but my understanding is newport only supplemented ketones and did not change his diet. My observation working with the elderly especially cognitive impairment is they eat tons of carbs very little meat or fat. They lose their appetites and are given small frequent snacks of easily digested starch or sugar because it's all they will eat. Part of their self care neglect involves wt loss and lack of food intake, so I actually strongly suspect newport was eating quite a carb based diet for this reason...all the more so wt loss was one of his symptoms (suggesting he was particularly sensitive to the lack of feeding as part of mental impairment). It might be his ketones were relatively high because he was declining so much and hypocaloric even on a very carb based diet he was perhaps dipping into keto slightly
This brings to another point, weight loss and failure to feed is part of dementia so a ketogenic diet may be particularly difficult to impliment , risk of death/infection from undereating may be greater than benefits to cognition. But newport doesn't seem that far gone yet and he is likely a candidate for a real ketogenic diet assuming his wife is mindful to force him to eat regularly and take supplements to prevent deficiency.
For seizures the keto diet takes about a week to kick in and a week to lose, the metabolic adaption to a very low carb intake is mechanism of action.
Whipped heavy cream + splenda = way tastier than most ice creams BTW
People tend to think keto is like paleo or weight loss style atkins and the food is bland , actually tons of fattening hedonistic things are perfectly keto.
Peter wrote: I have been unable to tease out, from Dr Newport's original article, that of Emily Deans or from the abstract of the case report above, quite what level of carbohydrate Mr Newport consumed in the original MCT phase, during the drug trial or while on ketone esters. I suspect it might have been more than a banana a day.
In their original trial in 2008
it was quite a lot more than a banana a day:
We put it in oatmeal, combine it with salad dressings, use it to
cook with, and put it on anything that one would normally put butter on, such as potatoes, sweet potatoes, rice, pasta or noodles. Coconut ice cream can be purchased at Asian stores, contains coconu oil and is the most pleasant way I can think of to make ketone bodies. Likewise, coconut milk is a combination of coconut oil and coconut water and can be found in the Asian and condensed milk sections of many grocery stores. It is a pleasant substitute for milk, and can be added instead of milk, for example, to make scrambled eggs, French toast, and mashed potatoes.
My sense is that their household is still wedded to the satfat/heart disease/unpalatable diet mindset. Nonetheless, great results from feeding the brain ketones.
Interestingly Dr. Vincent Tedone's mouse study for the Deanna Protocol for ALS suggested that the DP worked best without the ketogenic diet. I have several doubts about this (#1 being that they used mice in the study), but the question will probably come up again
Ketosis as a way of life.
"There’s a new article out in ASHG that discusses a regional selective sweep in CPT1A, carnitine palmitoyltransferase 1A, which plays an essential role in fatty acid metabolism. A mutation has become extremely common, with a gene frequency > 50%, in northeast Siberian populations, Eskimos, and Aleuts. This happened even though the c.1436C>T mutation has some negative side effects, such as reduced fasting tolerance and, apparently, a higher risk of infant death"
All the successful anecdotes I've heard for Alzheimer's have used a modified ketogneic diet, <100g carbs (usually <70) with MCT/coconut oil supplement.
Aye, I'm wary of this ability to influx your system with exogenous ketones, even for a newbie carb-dodger much of the self-generated ketones are wasted - I'll need to see decent data on actual utilisation to have a real idea on whether they're useful or not.
Probably, the easiest way to create a variety of LC fatty foods is mixing already existing products which contain a sugar substitute like Yoplite with whipped cream or a mascarpone cheese. Bakers chocolate is another ingredient with a great potential to be the base for a tasty treat like a truffle for an elderly person. Supplements could be incorporated into truffles for seniors who have a trouble to swallow big pills.
I made an error in my last posting and could not edit it. SO here is the fix. Dr. Grossman is the NS at Hopkins who tracked patients during their treatments for GBM with Temodar and XRT (standard tx these days). What was not standard was they began to follow BG levels while statistically accounting for Decadron use, and he broke them in quartiles to see if he could gain any insight. To many of the NS and oncologist surprise he found group down with a blood glucose had a huge benefit in survival when BG was less than 92. His other study was more impressive to me because it showed in patients being treated for GBM with Temodar and XRT, just 1-3 spikes in their blood glucose over 180 decreases their survival by 6 months. Survival in this group is only 1 yr in the NS literature.
1.Grossman SA, Ye X, Chamberlain M, Mikkelsen T, Batchelor T, Desideri S, Piantadosi S, Fine H.Talampanel with standard radiation and temozolomide in patients with newly diagnosed glioblastoma: A
multicenter phase II trial. J Clin Oncol. 2009; 27:4155-61. PMCID2734427.
2. Grossman SA, Ye X, Piantadosi S, Nabors LB, Rosenfeld M, Fisher J. Survival of patients with newly
diagnosed glioblastoma treated with radiation and temozolomide on research studies in the United States.
Clin Cancer Res 2010. PMCID2861898
I agree Ash that exogenous ketones never will trump endogenous creation of ketones but in GBM and most brain diseases they are likely to be quite beneficial due to the Crabtree and Warburg effects as Peter mentions. Ketosis in the brain is all about closing the BBB and making neurons avoid the insulin pathways like AMPK and mTOR. Another exogenous Rx here with ketone esters is metformin: If you increase insulin sensitivity or Rx Metformin for the patient, you up regulate the AMPK pathway and you block mTOR as well. The effect however depends upon the redox shift in the mitochondria. When AMPK is up-regulated, it inhibits several insulin mediated pathways. Studies in humans have shown that the diabetes drug Metformin can activate AMPK. The same holds true for HIIT and glycemic carbohydrate restriction. AMPKis also a pathway that’s up regulated during stressors like a lack of food or when neurons exhibit calcium efflux for any reason. Hypercortisolism is classic. This is also true when the PVN is overstimulated by the environment while the grey matter vagal centers are under active. This happens when the BBB is opened. Nora Volkow's and Allan Frey's research have shown us this. When we artificially IF we tend to activate AMPK as a protection mechanism. So there are many ways to artificially activate this pathway exogenously. I still think using endogenous pathways are best when our mitochondria are not redox shifted. In Cancer, mental disease, and neurodegeneration we do not have that luxury in my opinion. 1.Derr RL, Ye X, Islas MU, Desideri S, Saudek CD, Grossman SA. The association between hyperglycemia and survival in patients with newly diagnosed glioblastoma. J Clin Oncol. 2009; 27:1082-6. PMCID2667812
This is the first time I comment on your blog. I found it through another blog and I'm really enjoying so much slowly reading all your posts.
I'm still not sure Paleo is good for me but I'm slowly increasing my fat intake and decreasing carbs and seeing how it goes. So far so good.
Anyway, I've read you eat lots of yolks and butter, then offal and cheap beef, etc.
But I haven't found (yet) your opinion on Organic sources for those foods. What's your relationship with organic food sources ?
Fat is supposed to get attached to nasty chemicals, heavy metals, PUFA's and so on. Or not ? Please illuminate us.
Aren't you concerned about toxic chemicals stored on aniamals offal ? Even if they are organic, if they are fed GM soy, corn, and so on ... Wouldn't that be bad for us ??
Thanks in advance.
Hi Valerie, that’s an interesting thing to try. A bit like long chain vinegar… With long chain FFAs I would expect them to be re esterified in the intestinal lining, but you don’t always get what you expect, so interesting effect on hypertension.
Galina, yes, though we all have to go of something, better feel as good as practical in the process!
Amy, thanks for the paper. BTW My feeling about apoE4 is that if you carry this gene you have no tolerance of carbohydrate, never mind the multiple other issues you run through in your thesis.
Lacie, my worry is that I have no idea what the ketogenic diet contained, “Animals in the KD group received a custom-designed diet with a macronutrient profile similar to the clinically prescribed KD” does not hack it in a scientific paper. And Table 1 tells us 77% of calories from fat. What sort of fat? Does MCTs vs ghee vs corn oil make any difference? Perhaps if I wanted to repeat the study I might need to know… I’m underwhelmed by the methods section of the paper and that worries me when I look at the author list. This should have been pulled up at scrutineering.
Emily, interesting. It seems like ketone esters get you out of this need for carbohydrate restriction. The MCTs appear to be a trade off of lowered glycaemia at the cost of elevated insulin. An FFA based milieu under hypoinsulinaemia has the biochemical appearance of a much better option. Clearly 70g or real food carbs per day plus some MCTs represents a massive improvement on the SAD, there looks to be scope to improve on it further…
Jack, will have to get those refs. BG around 140-180mg/dl seems to be where the sh!t hits the fan in degenerative diseases….
Marcus, I came here through VLC eating as core with nutrient dense foods as core. The organic aspects seem to come down the list. Hormesis has been shown for virtually every toxin examined. The question eventually becomes what is the dose rate in excess of hermetic benefit. That old “whatever does not kill me makes me stronger” has an addendum (from Malcolm Kendrick, I think) “so long as it doesn’t cripple me for life”.
Oops, got to go get breakfast for the family…
Oops, hormetic, not hermetic, we can leave the double glazing out of this!
Thanks for your answer. Sorry I'm not sure I get what you mean.
You mean toxins found in non-organic food can be beneficial if they're below a threshold (hormetic threshold) ?
Or you mean that you're going to get toxins either in organic and non-organic and that the hormetic threshold means that more toxins in the non-organic aren't necessarly worst that less toxins in the organic ?
Sorry I'm not an expert.
I'm thinking about arsenic fed to chicken, hormones and antibiotics fed to cattle, etc.
I'm not sure if long-chain FFAs act like vinegar. I think short- and medium-chain FFAs are treated differently from long ones. Not sure.
As to the fate of long-chain FFAs, I too would expect them to be re-esterified... if you have a glycerol molecule. But on a zero-carb diet, where does the glycerol come from? Blood glucose? If so, the digestion of FFAs would force glucose out of the bloodstream, so it should lower insulin, so it should lead to Good Things. Right?
I guess my next experiment would be to stick to a zero-carb diet, and test my BG before and after FFAs, compared to neutral oil. This all sounds very unpleasant.
Marcus, I feel LC produces huge benefits. Going organic may add to that but I doubt it is anything like the benefits of LC per se.
All toxins, at a low enough dose rate, appear to trigger repair processes with long term benefits. Knowing when you might exceed the hormetic dose rate is the difficult problem.
Thanks Peter! I get it now.
Cognitive decline Reversal
I think its the context that matters.
This paper puts MCT last on the list of 25 anti inflammatory protocols that together may improve cognitive function in the early stages of dementia.
Unfortunately the damage that produces the Alzheimer's cascade may occur 20 years or more before symptoms are diagnosable. So the time to start prevention strategies is sooner rather than later.
Just for kicks I finally decided to check what that annoying troll-promoter for his "healthy"web-site jobair rafi pushing on people who are interested in nutrition. The usual useless at the best cookie-cutter blabbing which travels from one "healthy" rug to another.
"If you run, jog, row, or do circuits as part of your cardio exercise, you might want to get most of your calories from carbohydrates. Carbs provide your muscles with glycogen, a form of energy that helps fuel your workouts and keep you going for longer. Good sources of carbohydrates include whole grain breads, pastas, rice, cereals, legumes, and fruits." Running on legumes sounds like an interesting idea.
No wonder he is trolling out of a desperation, even though I am sure he could list several pages of references to support his outdated recommendations. Please, don't click on his site in case he wants to generate clicks.
Hey Peter, have you read this about a possible cure for cancer (not diet related):
Ted, yes, I would put MCTs well below normoglycaemia in my quest for neural wellbeing. You can undoubtedly do a world of good by dropping whatever puts your blood glucose above some random and individual (but low) value. A few ketones might help, especially if their mitochondrial biogenesis effects help normalise glucose with continued CIAB consumption, but icing on the cake compared to avoiding CIAB. And avoiding icing on any cake. And avoiding cake. Unless the cake is VLC ketogenic cheesecake. Mmmmm, must make more cheesecake....
Ken, thanks for the link. Remi has nudged me on Facebook about the same paper and it’s quite fun, with interesting follow on thoughts. Might try a post.
Galina, thanks for suffering on everyone’s behalf. I’ll delete the comments containing the link you are talking about now that I’ve got two minutes to attend to the blog. It always amazes me that people seem so click hungry. Must be all the carb loading...
I'd be super wary of chugging ketones without adaptation, you will be pissing them out like multivitamins, and ketones compete for excretion with uric acid in the kidneys.
To me that's just asking for gout flare ups in the short term and kidney stones chronically.
For the sake of correctness, and in case anyone wants to give it a try, I need to ammend a previous comment of mine. I stated that NEFAs are very irritating. Well, it turns out that *some* NEFAs are irritating, others are not (or much less so).
The last batch I made is edible by mouth. It doesn't taste really good, but it doesn't hurt. No irritation, or very little.
I bought lard from the cooking section of the grovery store. Lard does not contain the very irritating short- and medium-chain fatty acids that (I think) make coconut NEFAs untolerable. The ingredient list on the package says "lard, BHA, BHT, citric acid". The last three ingredients are antioxidants. That probably helps too, since oxidation products are said to be irritating and unpalatable.
I mixed the melted lard with NaOH to complete saponification. The next day, I remelted the soap and added HCl to neutralise completely the NaOH. I let it sit overnight, and the NEFAs solidified over the layer of salty, glyceroly water (that's the theory, at least). The end product tastes mostly like lard (not good, but not really bad either) and is not really irritating. I wouldn't say it is pleasant to eat, but at least I can imagine doing some self-experiments with it.
Never mind all the science, where's the recipe for this LC cheesecake? One of very, very few things I have missed over the last 3 years of LCMPHF.
I have to wonder about the effects of ketones in the backdrop of a high carb diet. It's possible there'd be a therapeutic effect apart from the replacement of carbohydrate with ketones. If the ketones caused a decrease in free fatty acids--maybe that could play out as an increase in insulin sensitivity? Similar to adding vinegar, or alcohol in the diet. Short chain fatty acids (acetic acid from vinegar) and ketones share with alcohol in that they provide an alternate fuel source for the brain, decrease gluconeogenesis, and decrease lipolysis. Insulin resistance could get sidestepped with a ketogenic diet, but maybe ketones could partially ameliorate insulin resistance when carbs are high--allow the brain to better utilize not just the ketones provided, but the glucose as well.
Peter's mutton followed by cheesecake post, including recipes for both.
Great - thanks very much for the link back to the mutton (yum!) & cheesecake recipes. I anticipate that the cheesecake will be a regular with us.
I have been eating Zero Carb for over five months and I find it to be the TASTIEST, EASIEST, HEALTHIEST Way of Eating EVER, and I wish I had discovered this in my youth.
My diet consists of 70/30 ground beef for breakfast and lunch (1 pound at each meal) and either a chuck eye or rib eye steak for dinner. NEVER gets old.
I have had so much healing, besides weight loss, that I believe most people would thrive on a Zero Carb Diet -- Eat Meat and drink Water to thirst.
Dunno what the ZC stuff has to do with anything, but congrats on discovering carnivory.
As to the original blog, I haven't been following the science much this year - do we have any new data on the outcomes of administering exogenous ketones to "adapted" vs "non-adapted" individuals?
(that's the stuff I was talking about being super interested in last year)
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