The official "ketosis/#veganketo" thread

What is the lowest blood glucose level you've ever had? - Ketogenic Forums (keto forums!)

d-beta-hydroxybutyrate vs l-beta-hydroxybutyrate

foods I like: cashew queso [IN GLASS jar], beyond sausage, acai berries, jarred kale, mushrooms, vegan sugar-free chocolate [eg Lily’s], macademia nuts/pecans > almonds > other nuts, avocados, olives, high-polyphenol EVOO (eg Kosterina), tapenade, tofu, bok choy/endives/broccoli rabe/celery/chard >> other veggies, oat fiber, shirataki noodles/konjac, seaweed, nut milks/soymilk,ThinSlim bread, and [yeah] I guess shellfish/crustaceans [though avoid the non-veg* options in favor of veg* when possible]

Watercress/chard/chicories (like endives/escarole) is the best (also very filling and high in nutritional density). The Best Keto Vegetables List - The ultimate Low Carb Vegetables Guide

Rarer: cauliflower hummus
Macedonia [Vitalia] - Home | Vitalia Healthy Food - has special keto granola that’s cheap ( In Europe, there is a wide variety of fake meat/tofu of different brands

It is IMPORTANT to note that nutritional deficiencies can be WAY higher on keto, so get Vitamin supplements, and potassium electrolytes (why aren’t there potassium keto esters yet?)

POSSIBLY SGLT2 inhibitors/metformin are good on the edge (as is anything that could lower blood glucose levels on sum [which may be enough to KEEP you in ketosis in “edge” cases in enough instances to matter, and when doing keto there are A LOT of edge cases])


On BHB esters: (The Definitive Guide to Ketone Esters and Ketone Salts - Perfect Keto | Top 7 Exogenous Ketone Supplements (Based on Science))

Ketone salts (usually in the form of D/L-BHB salts).
Non-ethanol alcohols (usually in the form of (R)-1,3-butanediol).
Ketone esters (usually in the form of a bond between D-BHB and (R)-1,3-butanediol).
A combination of D-beta-hydroxybutyric acid and (R)-1,3-butanediol.

The difference between the first three has to do with how the ketone bodies are chemically bound to alcohol or salts.

Salts are much easier to manufacture, which is why most exogenous ketone supplements on the market are sold as salts. The problem with salts is that they can lead to stomach cramps and GI irritation, which is why I try to avoid them.

Plus, it’s worth noting that the only bioavailable form of BHB is D-BHB. As a result, products that contain a mix of both L-BHB and D-BHB are usually less effective (depending on the dosage) than products that only contain D-BHB.

Eric Verdin says the salts are worthless [they only work for 1 hour]. Eric uses Science Behind Metabolic Switch Ketone Ester – Juvenescence . His product is this - Metabolic Switch® Powder – Juvenescence. He mentions the book ketotarian ( )

getting into ketosis does not mean keto-adapted (it takes longer for cells to make the transcriptomic adjustments to be properly keto-adapted). Still trying to find academic papers for the “epigenetics/transcriptomics/proteomics/chromatin structure/post-translational modifications” of ketosis (there’s indication that the alterations to chromatin structure could be longer-than-temporary if you do it for long enough)

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is understood that reactive oxygen species (ROS) cause structural and functional damage to mitochondria, and that nutritional ketosis decreases mitochondrial ROS production. This could result in a prompt increase in the lifespan of existing mitochondria. Given estimates that mammalian mitochondria have half-lives in the 1-2 week range, and since it takes about 5 half-lives to reach equilibration after a change, an increase in mitochondrial lifetime might take 5-10 weeks to reach a new steady state for enhanced mitochondrial density, depending on the tissue or organ in question.

Is this thread for keto in general or only vegan keto? Sorry I just wasn’t sure and I’m keto but not vegan.

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Just veg* keto. I’m veg* so this just makes everything easier here. Anyways, too much protein is enough to kick one out of a ketogenic state, which means veganketo might be easier to do than meat keto

General posts about ketosis and its benefits are okay

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What Is the Cyclical Ketogenic Diet? Everything You Need to Know | What is the Cyclical Ketogenic Diet (CKD)?| Bulletproof

  • imilarly, cyclic ketogenic diet (every other week) prevented obesity, reduced midlife mortality, and prevented memory decline as mice age [38&]. At the gene expression level, cyclic ketogenic diet downregulated genes involved in FA synthesis, mechanistic target of rapamycin/ribosomes, and insulin pathways similar to nonketo-genic high-fat diet, but cyclic ketogenic diet uniquely upregulated peroxisome proliferator-activated receptor alpha target genes across various tissues [38&]
  • Newman JC, Covarrubias AJ, Zhao M, et al. Ketogenic diet reduces midlife mortality and improves memory in aging mice. Cell Metab 2017; 26: 547–557.e8.

Get a CGM if you do this [impt to monitor glucose spikes during break days]. They might not be so bad if you use acarbose + beans (I don’t know a single person who has tried it - people on are not the most open-minded)…

[I have been browsing ketogenicforums as of late - sadly most people do not seem to be scientifically enlightened (or truth-motivated).


  • A 2019 study
    published in Nature showed that a ketogenic diet upregulated the
    expression of __PPARGC1a __and FOXO1a in human and mouse T-cells.
    These two genes are important regulators of lipid and glucose metabolism (3). __PPARGC1a __is particularly
    important because it promotes fatty acid oxidation and the formation of new
    mitochondria in the cell.
  • The authors of
    the study found that a ketogenic diet increased beta-hydroxybutyrylation of
    these genes and caused their chromatin structure to open and increase gene

From Neuroketotherapeutics: A Modern Review of a Century-Old Therapy (10.1016/j.neuint.2017.05.019)

increasing β-hydroxybutyrate levels inhibits histone deacetylases (HDACs) 1, 3, and 4 and consequently increases acetylation of key histone residues. This acetylation enhances FOXO3A-mediated gene transcription. A subset of the effected genes includes those responsible for mitigating oxidative stress such as manganese superoxide dismutase (MnSOD) and catalase (Shimazu et al., 2013). Similarly, in vitro exposure to β-hydroxybutyrate promotes activity of the EP300 family of lysine acetyltransferases (KATs) (Marosi et al., 2016). Since ketones appear to modulate a number of enzymes that control the cycling of protein acetylation in the cytoplasm and nucleus, it is likely that ketones alter other compartments in a similar manner. Ketones could influence activity of Sirtuin 3, the major mitochondrial deacetylase, especially considering their recognized trafficking into the mitochondrial matrix (Rardin et al., 2013).
Another exciting recent development in the area of ketone body-PTM relationships is the discovery that β-hydroxybutyrate itself can modify lysine residues (Xie et al., 2016). β-hydroxybutyrylation of histone lysines produces gene expression changes that recapitulate those of histone acetylation. TCA intermediates generated during ketone body metabolism-associated reactions may additionally function as epigenetic modifiers. In particular, changes in protein succinylation that arise through the actions of α-ketoglutarate dehydrogenase, or other succinylation enzymes under ketotic conditions, are suspected (Gibson et al., 2015).

In the liver, when an excess amount of acetyl-CoA is produced that exceeds the availability of oxaloacetate and the activity of citrate synthase to enter the TCA cycle, acetyl-CoA is used for the biosynthesis of ketone bodies. Ketone bodies are produced via a rate limiting enzyme, 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2; see Box 1), in the hepatic mitochondrial matrix and transported into various tissues via circulation. To cross the membrane, ketone bodies are exported from the liver and imported to extrahepatic tissues via monocarboxylate transporters [4,5]. In contrast to acetyl-CoA, which is a highly hydrophobicmolecule, ketone bodies are water-soluble and do not need specific carriers for transportation. In particular, in contrast to the skeletal muscle and myocardium that can directly use fatty acids as an energy source, the brain cannot use them, necessitating the uptake of circulating ketone bodies into the brain under limited glucose availability. Once transported to each organ, ketone bodies are again converted back to acetoacetate by BDH1 and then to acetyl-CoA by 3-oxoacid CoA-transferase 1 (OXCT1), which is finally used as a local energy source [3]. Notably, β-OHB is not utilized by the liver because OXCT1 is absent there [6]. Thus, the primary role of ketone bodies is to act as substrates for energy production, and a KD recapitulates a pseudo-starvation metabolic state. (this is a good article)


Ketogenic diets inhibit mitochondrial biogenesis and induce cardiac fibrosis

This was a rat study using a terrible diet that happens to be keto. One could just as easily construct a terrible vegan diet that gives rats heart disease and then title it “vegan diet causes heart disease”.

They fed rats a diet that was 60+% cocoa butter

^oh crap, I’m using a lot of chocolate [it’s much more filling per calorie than nuts] (Eric Verdin is an author). This paper I really like

via deacetylation [139].
This provides a fascinating example of how multiple
metabolically-responsive pathways (e.g. SIRT1 and βOHB) might intersect
to provide overlapping epigenetic regulation: while βOHB inhibition of
HDAC2 may be broadly beneficial, the potentially detrimental inhibition
of HDAC1 by βOHB is offset by SIRT1 activation. Such cross-talk may be
common, where fasting-activated sirtuins provide tissue- or
subcellular-specific fine-tuning of the broad effects of βOHB.
Alternatively, different target specificities of class I and class III
HDACs could provide ample opportunity for coordinated regulation or
targets, even perhaps via different lysines on the same protein
. It
remains to be determined if inhibition of HDACs by βOHB has similar
effects on learning and memory in rodent models as chemical HDAC
inhibition or genetic manipulation, and precisely how HDAC inhibition by
βOHB intersects with other fasting-related mechanisms of epigenetic


(this from Eric Verdin, cyclic keto)

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My main concern with keto has always been methylglyoxal. Seems like post-2017 papers show that acetoacetate helps buffer it

hmm - Dear Mark: Ketosis and Methylglyoxal, Microwaving Vegetables, the Role of Salt in Cooking, and More Veggie Ideas | Mark's Daily Apple

f minor note, a small portion of acetoacetate undergoes non-enzymatic decarboxylation to form acetone (Kalapos, 2003) (Figure 2). Acetone, while toxic in large concentrations, undergoes liver conversion via the methylglyoxal pathway. As acetone is highly volatile, when acetone production rates exceed conversion rates it is readily excreted by the pulmonary system. As a result, it does not reach appreciable levels under states of fasting or nutritional ketosis.

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Mice overeat on a ketogenic diet so they cycled

A parallel paper (no cycling) increased longevity

Memory enhancement

Verdin created a new supplement recently

Ketosis interferes with class I HDACs (can improve memory - eg HDAC3 inhibition) but sirtuins are class 3 HDACs. Valproic acid is HDAC inhibitor that can work on epilepsy too

He’s against standard ketosis salts sold on Amazon (I tried those, they never helped)

Hyperacetylation on good sites like FOXO3

I spent all day researching this today I hope it’s all for now

Some ppl can’t do PPARalpha. PPARalpha is what isn’t upregulated in high fat alone. Some ppl increase protein to compensate but this is bad if top much

He published another paper that was negative on PBMC telomere length from CR… he was negative on CR this isn’t smg I agree with… (but REALLY PBMCs are not all cells… IF anything this may mean that PBMCs are not the best measure on aging for the CR diet)


he says “low histone acetylation helpful” (but doesn’t ketosis cause histone hyperacetylation at
tes like p300 and FOXO3?)


just search youtube more for eric verdin (eg ARDD2022). Older mice on ketogenic diet have STRONGER memory than non-old control mice…

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Eric Verdin mentioned this

A KD decreased hepatic levels of phosphorylated and total acetyl-CoA carboxylase (ACC), while increasing those of carnitine palmitoyltransferase 2 (CPT2) and medium-chain acyl-CoA dehydrogenase (MCAD) (Figures 2G–L). Phosphorylated and total pyruvate dehydrogenase (PDH) protein levels were also reduced by both LCD and KD (Figure 2H and 2K).

Total and phosphorylated levels of mTOR were not altered in liver by 1 month of LCD or KD (Figure 3A and S2). However, lower levels of phosphorylated 4E binding protein 1 (4E-BP1) and a similar trend for phosphorylated S6 ribosomal protein (rpS6) were detected, suggesting decreased mTORC1 signaling (Figure 3B and 3C) in liver. In contrast to liver, p-4E-BP1 levels were increased in the skeletal muscle of ketogenic mice after 1 month of diet (Figure S3). We also analyzed several signaling cascades modulating hepatic nutrient sensing by mTORC1. No changes were detected in phosphorylated AMPK, p-Akt or p-Erk1/2 between control and KD mice. Tuberous sclerosis complex 2 (TSC2) phosphorylation at S939 or S1387, as well as p-Raptor levels, were also unaltered by the KD (Figure S2). In contrast, levels of DNA damage-inducible transcript protein 4 (DDIT4, also known as Regulated In Development and DNA Damage or REDD1), a negative regulator of mTORC1, were significantly increased in the KD mice (Figure 3D).

Interestingly, it has been reported that p53 hyperacetylation inhibits mTORC1 in response to fasting by increasing the expression of DDIT4, a negative regulator of mTORC1 (Schupp et al., 2013). Moreover, this same pathway seems to mediate the effects of metformin (Ben Sahra et al., 2011). Our results, including increased p53 acetylation and DDIT4 levels and decreased mTORC1 downstream signaling, only in the ketogenic group are in accordance with this model. Of note, p53 hyperacetylation and stabilization may also be contributing to the marked decrease in cancer incidence in the KD mice. Cross-talk between HDAC inhibition and liver mTORC1 signaling is therefore a potential mechanism contributing to the longevity extension with a KD.

Acetylation has many important effects on p53. It increases p53 protein stability, binding to low affinity promoters, association with other proteins, antiviral activities, and is required for its checkpoint responses to DNA damage and activated oncogenes [39,40,41,42]. Six acetyltransferases have been identified that modify p53 at lysines predominantly in the C-terminus or its central DNA binding domain (Figure 3). Acetylation of p53 directly affects its transcriptional activity by opening up its normally closed conformation or by altering its binding to certain response elements in gene targets (Figure 4). In general, these modifications are mediated by two different groupings of acetyltransferases, p300/CBP/PCAF or Tip60/MOF/MOZ. There appears to be significant redundancy in sites of p53 acetylation since loss of one or more sites, including all seven C-terminal lysines in mouse p53, can be largely compensated for by acetylation of remaining lysines [43,44]. However, combined loss of eight major acetylation sites in human p53 (8KR mutant altered at K120, 164, 370, 372, 373, 381, 382 and 386) renders p53 transcriptionally inert and prevents its induction of cell cycle arrest and/or apoptosis [40]. Conversely, in many cell types the inhibition of histone deacetylases (HDACs) that remove acetyl groups from p53 (i.e., HDAC1 and SIRT1) causes increased p53 acetylation and p53-dependent activation of apoptosis and senescence

12.5g of ketone esters is… tiny… ( has a suggested dose of 12.5g - this is Eric Verdin’s supplement)

but it’s much higher than 2.5g of Frank LLosa’s ketone esters.

Whose ketone esters are better? How to convert to mmol/L?

If you’re interested in something vegan/keto friendly and bread like I made this recipe today.