I think your source has it wrong here. They are talking about exogenous ketone salts that contain the L-b-hydroxybutyrate molecule, which Veech et.al. do not recommend. [I think using Veech’s research to make their claim is morally questionable too, given his views on the subject.]
They can be partially used by the human body but they aren’t the natural form. The other study was using a L-/D- mixture given to rats.
See also: Keto Academy and Exogenous Ketones
[created a new topic for this]
Hmmm maybe source is wrong?
Would be kind of neat if source was not wrong?
Anyone care to write source and tell them they are wrong?
…lol
They have a laundry list of people who wrote that?
FOUND AN ERROR? LET US KNOW!
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Two research papers supporting claim of said endogenous production of D-BHB & L-BHB:
[1]http://www.jbc.org/content/252/15/5222.full.pdf (Note: this paper was published February 7th, 1977)
[2] Ketone Bodies Mimic the Life Span Extending Properties of Caloric Restriction: “…Ketone bodies were first found in the urine of subjects with diabetes (11) creating in physicians the thought that their pres- ence was pathological. However, Cahill showed that ketone bodies were the normal result from fasting in man (12), where they could be used in man in most extrahepatic tissue including brain (13). The ketone bodies, D-b-hydroxybutyrate (D-bHB) and its redox partner acetoacetate are increased during fasting (14), exercise (15), or by a low carbohydrate diet (16). Originally ketone bodies were thought to be produced by a reversal of the b-oxidation pathway of fatty acids. However, it was definitively and elegantly shown by Lehninger and Greville that the b-hydroxybutyrate of the b oxidation pathway was of the L form while that produced during ketogenesis was the D form (17). This fundamental difference in the metabolism of the D and L form of ketone bodies has profound metabolic effects. …”
[4] 3-hydroxyacyl-CoA dehydrogenase: Lehninger AL, Greville GD (1953). “The enzymic oxidation of alpha-and 2-beta-hydroxybutyrate”. Biochimica et Biophysica Acta. 12 (1–2): 188–202. doi:10.1016/0006-3002(53)90138-3. PMID 13115428
I found another sourced article about types of exogenous ketones, and the few studies I brought up were all tracing the path of D- and L- bhb following injection. I haven’t found any reference to endogenous production of D-bhb yet.
Typical experimental protocol*:
*Don’t try this at home
Looks like both D-BHB & L-BHB are endogenously produced? (…or can be?)
…also looks like this paper was originally published in the French language?
The enzymic oxidation of d- and l-β-hydroxybutyrate - Albert L. Lehninger & Guy D. Greville (1953)
Abstract:
Both dextrorotatory and levorotatory forms of β-hydroxybutyric acid are oxidized aerobically by suspensions of rat liver and kidney particles (mitochondria). However the data clearly indicate that the initial stages of oxidation of the two isomers are quite different in liver, although ultimately both isomers are oxidized via the tricarboxylic acid cycle. The enzymic mechanisms involved in the primary dehydrogenase of the two isomers were examined in clear extracts of acetone-dried mitochondria. It was found that the l -isomers causes the reduction of DPN+, presumably by action of the already known l -specific DPN-linked β-hydroxybutyric dyhydrogenase, which of course does not attack the d -isomer. The d -isomer also causes reduction of DPN+ but only if the extracts are supplemented with ATP, Coenzyme A, and Mg++. Evidence is presented that d -BOH is capable of forming a CoA derivative at the expense of ATP: ⤥The extracts contain a dehydrogenase catalyzing reversibly the reduction of DPN+ by d - β -hydroxybutyryl-CoA⤥. Reaction (1) is not stereochemically specific; both isomers form a CoA derivative. However the dehydrogenase catalyzing reaction (2) appears to be specific for d - β -hydroxybutyryl-CoA.
The metabolic significance of the pathways taken by the two isomers of β-hydroxybutyrate are briefly discussed. …More
Yes, the D- isomer is definitely metablozied when administered (though with less energy yield) else they wouldn’t be studying it or using it for anything. As to its being endogenous though as the sellers of ketone salts allege, still not seeing it. Cannot find a mention of it being found human or animal that hasn’t been treated with ketone salts first.
Although the L-isomer has been commonly regarded as the “naturally occurring”
form, some evidence exists that the d-isomer undergoes biological utilization. In 1902
McKENzIE demonstrated that the d-isomer is metabolized by the intact dog…
So, following the dog study reference as [7] Dakin 1910 (didn’t see a 1902 study by Daikin), we find they are injecting the dogs with… you guessed it… ketone salts.
If aceto-acetic acid in the form of its sodium salt be injected intravenously into
cats or dogs, a reduction occurs of a considerable part of the salt with formation of laevo-rotatory ,B-oxybutyric acid which is excretedin the urine. http://www.jbc.org/content/8/2.toc
Interesting footnote:
Can we go back any further than this ^^ one in the paper trail? 
Wait, I just noticed you added something to this post… looking
The only thing I could find mentioning D-bhb in the Krebs lecture from 1959 was this diagram:
… with the reference to a mysterious “another pathway” Lynen 1958. They were studying salts up until then? Google shows Lynen 1958 is referenced in a boatload of other papers, but the original title is eluding me.
In 1953, they concluded it was “probable” that D-bhb was of natural occurance. Again, tests using exogenous D-salts found it was metabolized through a different pathway but not proof it is created endogenously. If the probable conclusion has been proven since then, shouldn’t there be a paper stating such?
In this communication we wish to present data obtained employing the pure stereoisomers of B-hydroxybutyric acid which delineate the different enzymic pathways taken by the two forms. From these findings it appears probable that the d-isomer is also of “natural occurrence” and that it plays a role in ketone body and fatty acid metabolism.
…
Resolulion of dl-B-hydroxybulyric acid. dl-B-hydroxybutyric acid, prepared from the sodium
salt (British Drug Houses), was converted into the calcium-zinc double salt …
I’m sitting here thinking about this and there are many things interconnected with this subject, what is interesting to note is they use those exogenous ketones in military applications like for Navy Seals (my grandfather was one of the first Seals; frog men) and NASA astronauts. Another amazing fact is Shamans from indigenous cultures around the world use to use the urine of humans with diabetes (e.g. saami lampladers piss…ancient form of bullet proof coffee), yes ancient humans use to get diabetes (also possibly congenital Type 1 from birth?) but it was so rare you were considered an oracle (ketoacidosis) because of your urine, and also the urine from animals and extract the ketones from the urine by simply and mildly cooking it under a small flame to make a thick black tar like substance and place it into pine tree bark or needles tea (place a small dab in it); they would use this before going into battle or hunting for super human energy and strength like e.g. ancient berzerkers…lol
Still trying to piece this organic endogenous production of D-BHB & L-BHB together in my head from what I know so I will update this post in a few…
Endogenous production D-BHB & L-BHB:
This is a super complex subject so this might be merely speculatory?
The very ending word “butyrate” means BUTTER or the short chained fatty acids that certain gut bacteria make and ferment when you eat Resistant Starch e.g. HAM:RS2 or when you eat GRASS FED butter.
image sourceThis endogenous production of D-BHB & L-BHB may revolve around butyric acid, fermentation in the gut in contrast to INSULIN secretions and dipping into unexplored territory?
Pathway of D-BHB:
butyrate→butyryl-CoA→crotonyl-CoA→β-hydroxybutyryl-CoA→poly-β-hydroxybutyrate→D-β-(D-β-hydroxybutyryloxy)-butyrate→D-β-hydroxybutyrate[4]
Pathway of L-BHB: ?
Related:
[1] Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes.
[2] “…High anion gap. The anion gap is affected by changes in unmeasured ions. In uncontrolled diabetes, there is an increase in ketoacids due to metabolism of ketones. Raised levels of acid bind to bicarbonate to form carbon dioxide through the Henderson-Hasselbalch equation resulting in metabolic acidosis. …” …More
[3] Relationship Between Hydroxybutyrate and Acetoacetate Plus Acetone Contents of Blood and Urine of the Ruminant: Animals: Experimental Procedure: Mature female Saanen goats were used as experimental animals throughout the studies. To create states of hyperketonemia, goats were infused with butyric acid during metabolic states characterized by hypoglycemia. The hypo- glycemia was created by phlorizin treatment or by fasting the goats in late pregnancy. Details of the experimental methods have been published (6, 7). …” “…In the present study, more of the values for both the blood and urine ketone fractions were within the normal physiologic range than in Reid’s study (8), which might account for the differences noted. Based on our data, it would appear that above a blood or plasma concentration of B-hydroxybutyrate or acetoacetate plus acetone of 2 mg acetone/100 ml, a large increase in urinary concentration or excretion of the respective fractions occurs. Most work with monogastric animals indicates that both acetoacetate and B-hydroxybutyrate have urinary threshold levels (5, 14, 15), while acetone does not (15). The present study indicates that both urinary B-hydroxybutyrate and acetoacetate and acetone excretion increase with increasing blood or plasma levels, and above a whole blood or plasma concentration of 2 mg /100 ml, expressed as acetone, large increases in urinary concentration and excretion of both ketone fractions occur. At low concentrations of ketones in either blood or urine, B-hydroxybutyrate appears to be the major ketone body. Similar data obtained by Schultz and Myers (10) and Thin and Robeison (12) with cows showed a de crease in whole blood or plasma B-hydroxybutyrate :acetoacetate plus acetone ratios with increasing total ketone body concentration. In the present study, the de- crease in this ratio in whole blood, plasma, or urine occurred below total ketone body concentrations of 4 mg acetone/100 ml, and the ratio plateaued at a value of 2-3 above this concentration. The reason for this decreased ratio remains to be clarified, although it may be related to a decreased carbohydrate utilization due to hypoglycemia, which characterized the ketotic states reported in this study (6, 7). …More
[4] “…Butyrate can also be metabolized into D-β-hydroxybutyrate via a second metabolic pathway that does not involve acetoacetate as a metabolic intermediate. This metabolic pathway is as follows:[3]
The last reaction in this metabolic pathway, which involves the conversion of D-β-(D-β-hydroxybutyryloxy)-butyrate into D-β-hydroxybutyrate, is catalyzed by the hydroxybutyrate-dimer hydrolase enzyme.[3] …More
Sweeet, sweet urine. 
I knew they diagnosed diabetes that way, but I didn’t know it was considered a delicacy.
I feel kind of Shaman-like sometimes. I think the fasting practiced in several religions points to a state of ketosis too.
The D isomer or isoform of D-BHB comes from buytric acid (short chained fatty acids SCFA’s) produced endogenously by the gut flora microbiome (if you didn’t kill them off or from eating grass fed butter); this type of butyrate smells like human body odor or vomit and the other source or form of BHB comes from acetoacetate (AcAc); both forms are converted by the liver into D-BHB, BHB and possibly L-BHB and all are inhibited by insulin, everywhere I look L & D seem to be used interchangeably despite slight differences being that of polarity?
Note: D-BHB & L-BHB: d (−) and l (+); dextrorotatory and levorotatory?
All produced endogenously despite research of injecting ester isomers or buytric acid in concentrated form in experimental models into animals or human consumption of exogenous ketones?
The 2 isomers are like mirror images. L being left handed molecule, D- meaning dextro or right handed. A racemic mixture contains both L- and D- . This is very important in protein structures because the wrong isomer can be either not used by the body or in some cases it can have adverse side effects (citation needed lol). Given that bhb is a signalling molecule in addition to an energy source, there’s no telling what downstream effects incorrect signalling might have or where the intermediary metabolites of the L- form might be going.
The example Richard uses is Thalidomide, which caused birth defects.
I’m trying to think of another example…
Here, read these for me.
Although they have the same chemical structure, most isomers of chiral drugs exhibit marked differences in biological activities such as pharmacology, toxicology, pharmacokinetics, metabolism etc. Some mechanisms of these properties are also explained. Therefore, it is important to promote the chiral separation and analysis of racemic drugs in pharmaceutical industry as well as in clinic in order to eliminate the unwanted isomer from the preparation and to find an optimal treatment and a right therapeutic control for the patient.
Veech: We’re testing it again but it’s my impression that you could actually precipitate Parkinsonian crisis by giving these racemic salts. In other words, you’re interfering with the metabolism of the D-form. You’re interfering the penetration of the D into of the brain. They’re competing for the monocarboxylate transport. You’re inhibiting that and you’re also metabolizing the isomeric form through beta-oxidation which if you go back, reduces Q, which is not what I want to do. I wanted to oxidize. PODCAST transcript
The militrlary exactly isn’t known for being over-cautious when experimenting on their guinea pigs. Esters would be more expensive but likely also better performing with less potential for unknown long term side effects.
Stephan Guyenet wrote this back in December 7, 2009 which fascinates me to no end:
Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance?
Some other interesting connections, my thoughts here are about exogenous supplementation and endogenous production of D- and L-betahydroxybutyrate/BOHB’s are that one is natural and organic and the supplementation of such (man-made isometric) is not (inorganic) just like supplementing with man-made vitamins (alters the course of natural biological pathways) rather than the right combination of micronutrients found in fruits, vegetables, grass fed meats (incl. dairy, organ and glandulars) free range eggs & poultry i.e. Whole Foods (not removed from their encasement or natural shell i.e. no chemical preservatives or additives) and fermented grains etc. are the right combination of many nutrients in just the right micro-nutritional ratios?
Footnotes:
[1] Phinney & Volek: “…Seen from this perspective, AcAc generated in the liver acts as a NAD+ donor for the periphery, whereas pure BOHB taken orally, to the extent that it is retro-converted to AcAc (Sherwin 1975), potentially deprives the periphery of NAD+. …” “…If given all as a single salt, 50 grams per day of BOHB would MANDATE daily intakes of 5.8 g Mg++, 9.6 g Ca++, 11.0 g Na+, or 18.8 g K+. Even if divided up carefully as a mixture of these various salts, it would be problematic getting past 30 grams per day of BOHB intake. And again, most of the currently marketed ketone salt formulations are made with a mix of the D- and L-isomers of BOHB, so the actual delivered dose of the more desirable D-isomer is considerably less. The other concern with the salt formulations is that, as the salts of weak acids, they have an alkalinizing metabolic effect that might have a modest but cumulative effect on blood pH and renal function . …” …More
[3] Effect of a Sodium and Calcium DL- β - Hydroxybutyrate Salt in Healthy Adults+
Nice footnote find… I’m going to stare at this for a bit…
https://www.genome.jp/kegg-bin/show_pathway?map00650
This part at the top is the pathway that the exogenous ketone esters use (butane-2-3-diol) which produces the D- isomer.
This part at the lower left corner metions R-3-hydroxybutanoate, which is the right-hand molecule D-bhb.
The poly-β-hydroxybutyrate is also a right-handed molecule.
PHB (also known as Poly-( R )-3-hydroxybutyrate) is a biopolymer consisting of linear chains of β-OHB (Figure (Figure1).1). Three types of PHB with different numbers of β-OHB units and with different functions have been discovered: (i) high molecular weight storage PHB consists of 10,000 to >1,000,000 β-OHB residues (storage PHB), (ii) low molecular weight PHB with medium–chain length consisting of 100–300 residues (oligo-PHB), and (iii) short-chain conjugated PHB (cPHB) in which low numbers of β-OHB residues (≤30) are covalently linked to proteins (see Reusch, 1992, 2012, 2013 for comprehensive reviews).
It is possible to make a totally right-handed salt, but the level of salt is way higher, thus the salts use a racemic mixture because… profit?
Dave: … The ketone salt is all a front. If a company came out with one that was only the D-form, what would you say?
Dr. Veech: Wow. How high can it get?
Dave: You’re saying there will just be too much salt and not enough ketone?
Dr. Veech: Yeah.
