Category Archives: Ketosis

Dietary protein, ketosis, and appetite control.

Dietary protein has a purpose, and that purpose is not carbs.”  Nor is it to break ketosis or stall weight loss.  

Drastically increasing protein intake may reduce the degree of ketosis in the context of a large energy surplus, but this is likely due more specifically to the large energy surplus than the protein.  This would explain why Warrior dieters (1 meal meal per day) often report reduced ketones if they eat too much protein.  It’s more likely that the 2000 kcal bolus is exerting it’s anti-ketotic effect by being a large energy surplus, such that anything other than 90% fat would blunt ketosis.  It’s not the proteins… Want proof?  Here’s an n=1 to try: give up Warrior dieting for a few days and try 3 squares.  My bet is that you’ll be able to increase protein intake and still register ketones as high or higher than before.  There are data to support this and reasons why it may not matter (below).

disclaimer: I don’t think “deep ketosis” is necessary to reap the benefits of carbohydrate-restriction.  But if you love high ketone meter readings, then this might be a better strategy to maintain deep ketosis while getting adequate protein. win-win.

if I hear: “oh no, I was kicked out of ketosis!” one more time… 

All of the studies below are confounded one way or another, but so are we humans.

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Implications of the circadian nature of ketones.

Ketosis.  Happens during starvation and also by restricting carbohydrates (and protein, to a lesser degree)… might be important for epilepsy and bipolar disorder, too.


Ketostix measure urinary acetoacetate (AcAc) and reflect the degree of ketosis in the blood probably about 2-4 hours ago.  Blood ketone meters measure beta-hydroxybutyrate (bHB) right now.  bHB fluctuates to a greater degree, eg, it plummets after a meal whereas AcAc takes longer to decline.  AcAc/bHB is usually around 1, but increases after a meal (Mori et al., 1990):Ketone body ratio

Conversely, when glucose levels decline and fatty acid oxidation increases, liver redox potential drops which reduces AcAc/bHB.

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All my organs hurt and I think I’m going blind.

People, this is how you should eat.

There have been a lot of diet postings lately, and they are some of the healthiest diets you could imagine.  Please click the links to get the full versions, which include lifestyle tidbits, other pearls, and WHY.  And take notes.  I’ve just listed some of the foods here for the sake of brevity (and as an excuse to link to the diets).

Disclaimer: all of these diets fall somewhere on the “low carb” spectrum.  I don’t eat low carb because I have to*, I do so because it’s healthy, convenient for my lifestyle, and I rather like the foods.  *I say I don’t “have to” because I have no underlying health problems or carb-sensitive GI issues.  The people below are also far healthier than most (from what I can gather)… but if you are overweight &/or obesity-prone, or glucose-intolerant &/or diabetic, then you might want to consider following any of them.

Hyperlipid (Petro Dobromylskyj)The Optimal Diet
butter, egg yolks, cocoa, dark chocolate, macadamia nuts, sour cream, beef, green veggies.  His stats: BW stable, 28” waist, greying beard.  Peter will outlive us all.  And take over the world if he ever has the desire to do so.

Anna Fagan (Lifextension): Low Carb Paleo, probably keto
eggs, butter, avocado, cheese, shrooms, bacon, salmon, tea, coffee, nuts, sardines, lamb, pork, eggplant, cream  –> “high fat =/= fat.”  She’s currently off studying paleoanthropology somewhere in Turkey (?).

Jane Plain (ItsTheWooo): Ketogenic
cream, sour cream, nuts, butter, beef & fatty meats, pepperoni.  She, too, is rather fit.  The Scribble Pad = diet & lifestyle vs. psychoneuroendocrinology & metabolism (mixed with equal parts humor & gravitas).

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Eating in the Absence of Hunger

Hat tip to Jane Plain and her ongoing series on “The physiology of body fat regulation” for citing this study as it provides a rather interesting insight into the psychoendoneuropathophysiology of the obese condition.  Eating in the Absence of Hunger.  

Caloric compensation and eating in the absence of hunger in 5- to 12-y-old weight-discordant siblings (Kral et al., 2012)

They were all full or half, weight-discordant, same-sex siblings and each sibling pair had the same mother; same mitochondrial DNA, shared a womb, etc.

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The curiosities of nicotin..ic acid

Niacin vs. ketosis

Part I.  Rodents

It is thought: niacin causes red itchy face (> 100 mg/d) and acutely lowers FFAs; chronically, it raises some questionable fraction of HDL (> 1000 mg/d) and probably causes diabetes.

It is speculated: niacin binds a particular “ketone” receptor (GPR109?) (physiological relevance?).

It is known: niacin is ketogenic in rats.  Repeat: niacin is ketogenic in rats.

Niacin aka nicotinic acid and nicotamide aka niacinamide both fulfill the requirement for Vitamin B3 (ie, prevent pellagra).  But only the former causes flushing… and only the former is ketogenic (two apparently unrelated phenomena).

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How to define a “healthy” diet. Period.

Whether you’re strictly adhering to a diet or just doing your own thing, if year after year your GP is prescribing more and more medications to stave off morbidity and keep you intact, then the diet you’re following is most likely Fail.  The same is true if your body weight is creeping upward or your quality of life is creeping downward.lunchables

The glaring Fail of all 3 diets in the recent Mediterranean Diet Study for the medications criteria threw up a huge red flag.  As a brief refresher, at baseline and 5 years later, prescription medication usage was as follows:

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Athletes who drop carbs cold turkey suddenly suck.  It is known.  

But with a smidge of stick-to-it-iveness, performance completely recovers, in virtually every.  measurable.  aspect.  

This was shown years and years ago, in a seminal study by Drs Phinney, Bistrian, Evans, Gervino, and Blackburn.

The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capability with reduced carbohydrate oxidation (1983)

Normally, fatty acids fuel low intensity exercise and carbs fuel high.  This is because high intensity exercise requires a high rate of ATP production, and glycogen to lactate generates ATP faster than a speeding bullet.  This is what makes power.  Getting ATP from fatty acids is like draining maple syrup from trees [at first].

mito pic

However, go low carb for long enough and the syrup begins to flow like water.  I lack the time to show what “long enough” entails, but  4 out of 5 studies on low carb diets and performance that only last a few days will show this.  Ketoadaptation takes time; ~3 weeks.

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This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.

Yes, I think sugar and empty calories, and the associated hyperinsulinemia are the bane of anyone with obesity or any sort of hyperplastic fat tissue disorder.  And yes, this is the worst type of evidence to support such a stance, but when you’ve got lemons, well…

Make no mistake, diabulemia may as well be spelled DIE-abulemia.  It’s not a laughing matter.  But yeah, well, lemonade, etc.  So here it goes


Type I diabetics have low insulin and are lean; type II diabetics have high insulin and are not.  Insulin injections in either population promotes hyperplastic fat growth.  Sounds scary, right?  It is:


This poor soul unfortunately restricted his insulin injections to only two sites.  Make all the jokes you want, but the effect is obvious…  this is happening everywhere in hyperinsulinemic heavyweights (not just two specific sites).

CHO III Picture 279

 So what do Type I’s do when they want to lose some fat mass?  Stop jabbing themselves with insulin. Unfortunately, it’s really that simple.  Type II’s and anyone with excess or hyperplastic fat tissue can do the same with low carb or keto, although this would be a great benefit to their overall health.  But for Type I’s… not so much – they need insulin to prevent the horrific manifestations of ketoacidosis, which includes but is not limited to: death.

Type I’s are hyperglycemic because of low insulin; insulin therapy prevents diabetic ketoacidosis, a deadly condition.  But for those who simply choose to selectively reduce their insulin dosage, they: 1) don’t die; 2) lose fat; and 3) get hyperglycemic and incur all the damage that ensues (retinopathy, nephropathy, neuropathy).  Furthermore, they’re walking on thin ice – DKA is lurking.  It is just as stupid yet more dangerous than using tapeworms to lose weight.


Type II’s are hyperglycemic because of insulin resistance; a condition that is pathologically neutered via carbohydrate restriction.  Type I’s who reduce insulin injections to decrease fat mass are doing just as much damage as Type II’s who DON’T reduce carbohydrate intake.

Diabulemia is akin to an eating disorder.  Biologically, the lack of insulin allows fat to be released from adipose tissue with gravitas, and it prevents glucose from being stored in any meaningful capacity.  You’re literally pissing calories here, burning ’em like crazy there; all of which is a helluva lot easier than “eating less moving more” … which is why diabulemics do it (because they have the option [unlike the rest of us]).  Diabulemia is good from a fat loss perspective, but will most definitely contribute to severe and possibly deadly complications down the line.   Carbohydrate restriction, however, is a win-win-win… (for everyone except The Man, so perhaps it’s a win-win-win… fail)

This isn’t a “magic bullet,” it’s a buckshot aimed at a barn door.

Humans aren’t big rats, but here it is again, anyway:

Leptin deficiency causes insulin resistance induced by uncontrolled diabetes (German et al., 2010)

I’m ignoring the brunt of this paper and only focusing on the positive control groups.  [Positive controls… meaning they were included because they would definitely exhibit the expected response.]

Force rats into a state of diabulemia, and their insulin levels plummet, blood glucose soars, and they become ravenously hungry (open squares in the graphs below).German I

But lo and behold, fat mass atrophy ->German II

Eat less move more?  Well, they certainly didn’t “eat less…” (see above) … and:German III

nor were they “moving more.”  Low insulin seems to have a way to bypass that whole “eat less move more” thing (eg, Metabolic rate per se).


Throwing the baby out with the bathwater works if the baby is fat and the bathwater is insulin.  (no, not a fat baby.)

calories proper


Insulin vs. fat metabolism FTW

Insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga.

Teaser: insulin-induce hypoglycemia can get deadly quite fast, and there is no equivalent for the effects of insulin on fat.  However, the effects of insulin on fat are 100 times more powerful.

Background: Hormone sensitive lipase (HSL) responds to insulin by inhibiting lipolysis.  It halts fat burning.  It got its name because it’s THEE most hormone-sensitive lipase in the body.  The hormone about which we are speaking is of course insulin.  And the enzyme, or at least one of the enzymes as it were, is HSL.  To be clear, it takes very little insulin to inhibit HSL.  Just a dollop, in fact.

Effect of very small concentrations of insulin on forearm metabolism.  Persistence of its action on potassium and free fatty acids without its effect on glucose.   (Zierler and Rabinowitz, 1964)

Expt 1.  Since we’re all about jabbing people with insulin lately, let’s get at it again.  Jab someone with about 100 uU (/min*kg), and muscle and fat vacuum glucose out of the blood.  Same goes for potassium; and adipose gets all stingy too… it stops releasing and starts storing fat.  This is “healthy,” and its part of why people say insulin, and by extension carbohydrate, causes lean people grow fat tissue.

What do you think would happen in an insulin resistant obese crowd.  Less glucose vacuuming, but scrooge adipose will still responds with gravitas, by saving more and spending less?  Likely.  HSL is like the little piggy’s straw house.  The strong young wolf can blow it down.  The COPD emphysema wolf can blow it down…  because it’s made of straw.

Thus, insulin causes lean people to grow fat tissue, and it causes obese people to grow more fat tissue.

In other words, with regard to common obesity, being resistant to insulin means postprandial hyperglycemia; you can’t handle sugars proper.  but it’ll still make you fat(ter).

Expt 2. The interesting part.  Try jabbing healthy people with 10x less insulin.  Looks like IR obesity!  Adipose gets stingy, potassium scrams, but no effect on glucose uptake.

In the figure below: A-DV is muscle; A-SV is adipose.  Glucose uptake into fat & muscle is unaffected by a low dose of insulin.glucose on 10uU

Second figure: with the same dose, adipose goes on a budget SAVE MORE SPEND LESSFAs on 10 uU

Conclusion.  In a healthy person, (eg, healthy person), even very low doses of insulin cause fat growth.  This isn’t an issue of high vs. low glycemic issue.  The insulin dose used in this study was less than that expected from a respectable low glycemic index meal.  This is probably why the glycemic index hasn’t cured the obesity epidemic.  On the other hand, dietary fat doesn’t stimulate insulin…  just sayin’

Furthermore, perhaps glucose uptake into adipose promotes fat storage under certain conditions, but it’s clearly neither necessary nor essential.  Insulin can Miracle Grow fat mass without affecting glucose uptake one iota.  I imagine the abundance of 3C precursors simply isn’t “the limiting factor.”  And it works just as good with Whole Foods Low GI pa$ta and Wonderbread.buttressed

Translation: insulin buttresses fat growth.  and it doesn’t matter how much.  FYI this probably seems nonsensical at first: carbs stimulate insulin in order to dispose of said carbs, like a logical feedback mechanism.  Perhaps.  But said insulin cares far more about fat than said carbs.  On a scale of 1 to 10 (ie, putting things into “perspective”): insulin is there to grow fat tissue for the obesity epidemic, not replenish glycogen after yoga.

Part II.

Dose-dependent effect of insulin on plasma free fatty acid turnover and oxidation in humans (Bonadonna et al., 1990)

There are a lot of data in this paper, but here are the relevant points:

Infuse insulin at various rates.  In the lowest infusion rate, the only aspect of glucose metabolism to respond is hepatic glucose production (second line; HGP declines from 2.0 to 1.34 at the lowest dose):glc turnover

WRT low dose insulin on glucose metabolism: liver responds, not skeletal muscle.  Skeletal muscle doesn’t even look at glucose until insulin infusion reaches 250 – 500 uU, which is probably why back in ’64 they saw absolutely no effect at 10 uU.  At 100 uU they saw an effect, but according to these data, it was likely due solely to liver, because skeletal muscle doesn’t seem to care until levels exceed 250 uU (it’s an infusion rate, not an absolute concentration.  But that’s neither here nor there).  To be clear, 10 uU insulin infusion doesn’t affect glucose metabolism (1964).  period.  100 uU modestly affects it (1964), and this is probably so modest because only liver is helping out (1990).  At 500 uU, full scale attack on blood glucose.

But fatty acids are obliterated with 5 – 50 x less:FA turnover

It worked with 10 uU in ’64, and it worked just as well with 100 uU in ’90.  (FYI the first paper was published in 1964; this one in 1990).

Furthermore, in the table above glucose metabolism was progressively affected with increasing insulin concentrations.  Not so much with FAs:FA suppression

FA flux is rapidly and completely shut down with a dollop of insulin.  Indeed, it is obliterated.  Giving more insulin doesn’t do anything, because, well, when you blow down a straw house, it tends to stay down.

calories proper


40 years ago a group of researchers turned ketosis into poetry.

But first, a brief primer.  In red.

“The glucose muscle-sparing effect of fat-derived fuels” 

or, the Randle Cycle 2.0.  it’s like a course in life enhancement.

Part I.  Intermediary metabolism

The glucose-fatty acid cycle
The Randle Cycle, as originally proposed, states that fatty acid oxidation inhibits glucose oxidation.  This is good because during starvation, every tissue than can survive on fatty acids instead of glucose should do so, sparing as much precious glucose as possible for the brain.

The glucose-sparing effect of fat-derived fuels
A critical vital horcrux to this is in the oh-so-humbly-disguised phrase “fat-derived fuels.”  The fat-derived fuels are ketones, and they are rescuing the brain from starvation (ie, neuroglycopenia); they do so by supplementing glucose as a fuel source.  Ketones are good at this; many tissues are happy to oxidize ketones when they are available.

The glucose muscle-sparing effect of fat-derived fuels
Ketones are derived from fat.  During prolonged starvation, glucose comes from skeletal muscle amino acids (eg, alanine).  Ketones spare glucose.  Thus, ketones spare muscle.  QED.

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