Dr. Darren Schmidt : Time To Update Your Keto Knowledge

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(Bunny) #41

Ketones are made from dietary fat or body fat (oxidative breakdown), ketones DO NOT burn fat?

I do wonder if the science on this is all that clear because those are ketones you can see, ketones are a byproduct of oxidation of lipids and the device used to measure them is finding trace amounts of them in the blood stream, so how do you really know how much is actually being used rather than excreted?

When I see what Richard is discussing below it makes me wonder how much of those ketones are actually being used vs. how many your seeing?

”…I suspect when we first start we aren’t good at using them so we make too many and use too little so we end up with a lot left in our blood. …More

Here is Richard and Carl doing a scientific experiment using an Ecal breathalyzer, demonstrating Carl is the better metabolic fat burner! Another way to measure this?

Richard Morris Metabolic Testing at Ketofest Down Under 2018


(Karim Wassef) #42

ketones are the signal that fat oxidation is occurring.

if you’re not seeing ketones in the blood, then either your consumption is EXACTLY equal to your generation - which is nearly impossible consistently… or you’re not using fat.

the body generates more than it needs when there is limited availability of glucose, because THAT’S where the energy storage goes when there’s low glycogen.

If it isn’t, then it has plenty of glycogen and doesn’t need to have ketones available. the higher my ketones, the more fat is being oxidized. It’s right there in the data.

please look at the data. I’ve collected thousands of data points that show this over and over. I’m not using breath ketones. I’m measuring blood glucose and blood ketones… five times a day.


(Karim Wassef) #43

Would anyone believe that there is a forest fire with zero smoke??

Seriously… the argument of fat oxidation without ketones is the equivalent of a perfect balance of fire that doesn’t release any smoke.

Ketones signal that fat oxidation is happening the way smoke signals that there is a fire.

Sure - the body can use fatty acids directly, but when it does, it also generates ketones. This is the low glucose, low glycogen state… fatty acids used now, ketones generated for use later.


(Karim Wassef) #44

Ketogenesis occurs primarily in hepatic mitochondrial matrix at rates proportional to total fat oxidation. After transport of acyl chains across the mitochondrial membranes and β-oxidation, the mitochondrial isoform of 3-hydroxymethylglutaryl-CoA synthase (HMGCS2) catalyzes the fate committing condensation of acetoacetyl-CoA (AcAc-CoA) and acetyl-CoA to generate HMG-CoA (Fig. 1A). HMG-CoA lyase (HMGCL) cleaves HMG-CoA to liberate acetyl-CoA and acetoacetate (AcAc), and the latter is reduced to d-β-hydroxybutyrate (d-βOHB) by phosphatidylcholine-dependent mitochondrial d-βOHB dehydrogenase (BDH1) in a NAD+/NADH-coupled near-equilibrium reaction (Bock and Fleischer, 1975; LEHNINGER et al., 1960). The BDH1 equilibrium constant favors d-βOHB production, but the ratio of AcAc/d-βOHB ketone bodies is directly proportional to mitochondrial NAD+/NADH ratio, and thus BDH1 oxidoreductase activity modulates mitochondrial redox potential (Krebs et al., 1969; Williamson et al., 1967). AcAc can also spontaneously decarboxylate to acetone (Pedersen, 1929), the source of sweet odor in humans suffering ketoacidosis ( i.e. , total serum ketone bodies > ~7 mM; AcAc pKa 3.6, βOHB pKa 4.7). The mechanisms through which ketone bodies are transported across the mitochondrial inner membrane are not known, but AcAc/d-βOHB are released from cells via monocarboxylate transporters (in mammals, MCT 1 and 2, also known as solute carrier 16A family members 1 and 7) and transported in the circulation to extrahepatic tissues for terminal oxidation (Cotter et al., 2011; Halestrap and Wilson, 2012; Halestrap, 2012; Hugo et al., 2012). Concentrations of circulating ketone bodies are higher than those in the extrahepatic tissues (Harrison and Long, 1940) indicating ketone bodies are transported down a concentration gradient. Loss-of-function mutations in MCT1 are associated with spontaneous bouts of ketoacidosis, suggesting a critical role in ketone body import.


(Bunny) #45

Looking at this below does not look like there would be a limited supply of glucose at any time even if your skeletal muscle is in glucose refusal mode, the glycogen or glycerol can be converted back into glucose if needed, it is too much sugar in the diet, not a lack of glucose that causes glucose toxicity then a fatty liver (hepatic insulin resistance)?

Let’s say your not eating sugar rich foods, for example Paleolithic era foods that were really low in sugar, now time warp into the here and now, you could still be in ketosis even though your not seeing them with a ketone blood meter because they are all being used? What if the ketogenic diet is the extreme end of the spectrum (forced ketoacidosis) because we are dealing with things we can’t see? Maybe we are pioneers in figuring out that it is not all visual from a machine?

Glycerol and glycogen turning into glucose?

Then you have lactate?

Then you have RBC’s that need a constant supply of glucose?

RBC’s Cellular processes: As a result of not containing mitochondria, red blood cells use none of the oxygen they transport; instead they produce the energy carrier ATP by the glycolysis of glucose and lactic acid fermentation on the resulting pyruvate. …More


(Karim Wassef) #46

RBCs always need glucose, so without carbs the body goes through GNG to make enough.
Cortisol also stimulates GNG to make glucose.

GNG can come from protein or fat. If it comes from fat, it pulls the glycerol backbone off the fat and releases three fatty acids.

The body can use glucose (and glycogen) and then it can use lactate (which is a biproduct of glucose metabolism, recycled). and then it needs fat oxidation.

All this is true, but it doesn’t change the fact that ketones indicate that fat oxidation is taking place?

Paleo that is low in sugar would also result in elevated ketones.

I have not seen any research that contradicts my personal data: if there’s fat oxidation, there will be ketone production and you can measure it in the blood.


#47

It’s the insulin that causes a decrease in ketones, followed by a compensatory increase in glucose to keep the brain happy. Ketones are like happy juice. :grinning:


(Karim Wassef) #48

Actually I think it’s a combination of insulin and cortisol.

GNG is generally demand driven and cortisol creates demand for glucose. In the absence of carbs, protein works - demand based.

However, with an abundance of protein, the insulin also plays a role with deamination of the AA once enough has been processed to support lean mass construction. There is no “protein” storage mechanism and the body won’t waste precious energy so it goes through GNG either to support a glucose need or it shuttles it into fat. This is only with excessive protein - supply based.


(Bob M) #49

I’ve sen no evidence of low ketones being bad. None. Zero. Zilch. For instance, see the following:

However, while high blood ketones (BHB) is often targeted as evidence of being “in ketosis”, BHB levels often typically taper off over time, especially if you are lean, active, metabolically healthy and weight stable.

It seems that as our fat stores become ‘less full’ we don’t store as much energy in the bloodstream. And, as we will see later, once our NAD+: NADH ratio increases, less acetoacetate is pushed off to into storage as BHB.

One of the most fascinating outcomes of the one-year Virta study was that over the period of a year, participants’ BHB levels went from 0.17 mmol/L to an average of 0.54 mmol/L after 10 weeks and then settled back to 0.3 mmol/L after a year.[[14]]

(https://optimisingnutrition.com/2018/02/24/is-the-acetoneglucose-ratio-the-holy-grail-of-tracking-optimal-ketosis/#_ftn14)

I have been low carb/keto 5.5 years now. I NEVER have ketones above about 1.0 mmol/L, and I have almost two thousand tests spanning more than three years, unless I fast longer than at least a day or more.

My morning blood sugar is about the same over the last three years.

My HbA1c continues to decrease.

If ANYONE has ANY evidence that lower ketones are “bad” (let’s ignore those who want high ketones due to, say, cancer), please show it. I have seen NONE.


(Karim Wassef) #50

They’re not bad, just don’t indicate high rates of fat loss. If you’re in high fat oxidation, ketones are high. If you’re in low fat oxidation, ketones are low.

You can lose 60lbs of fat in 3 months or three years… different rates of fat oxidation and ensuing ketone production. If you’re in low ketosis, you will still slowly address insulin resistance.

Most SAD are low ketone - so that’s bad, but because of high glucose and insulin suppressing fat oxidation… not the low ketones per se.


(Richard Morris) #51

31.5 ±6 kCal / lb of body fat/day.

It’s around 1% of stored energy per day. The limit is how fast adipocytes will give us energy. Not a lot of people know about it. I think it’s my unique task to bring this work from obscurity.

I had a senior lecture in biochem the other day mention that we have a virtually unlimited supply of energy in body fat. I asked “Then why don’t fat people self combust when they go for a run?”


#52

I just herked up my coffee. :joy:

Thanks for the number @richard and @Karim_Wassef (34kCal/lb) .

It really helps in the guiding mathematics to benchmark a step of the latest weight loss plateau. The maths is just a nerdy way to take the step. It’s not essential.

[For Australians: 56 to 82.5 kCal/kg of body fat/day.]


(Karim Wassef) #53

I’m running an iterative simulation on my thread for this. Check it out.

(Science nerd here too)