I am trying to get a zero ketones on my newer-model keto mojo. I tested two people over the holidays, both got 0.1. I ate an entire (real) pizza one night and the next morning got 0.1 mmol/l.
I meant to test someone I knew was a carb-centric (but thin) person, but I forgot.
Has anyone had a new keto mojo and gotten a zero on ketones?
I’d think that’s pretty normal, whether we’re primarily fat or carb powered, we always do still burn both. People still lose tons of fat on high carb diets, and when they oxidize fat stores they’d make ketones too.
I don’t know. I saw a study comparing cyclists on high carb and keto diets, and the high carb cyclists did make ketones, but not until they had ridden a ton.
I was just trying to figure out if I ever switch out of “ketosis” (my normal ketones are low, <0.5). But maybe I was out, but won’t get a zero?
As a fellow data geek, I appreciate that this may not be what you want to hear but: Consumer blood serum measurement devices - like the KetoMojo - at best provide ordinal metrics, not cardinal.
I’ve owned a Mojo for many years now. Trying to discern just how much my BHB might rise or fall based on things I’m eating or doing eventually gets frustrating (and costly).
When first starting out on keto, my Mojo confirmed that my BHB levels were skyrocketing - I got more concerned than pleased. Then slowly, apparently as I became fat-adapted, they settled into the “not much” zone where most of us long-timers find ourselves with such devices.
The fact is, as you well know, if you aren’t eating meaningful amounts of carbs - and you’re not dead - you’re definitely in ketosis. Just “how much” is a matter for your metabolism and homeostasis to resolve. You’ll go broke with Mojo strips trying to get much more precise of an answer than that. 
Still, I can relate to the urge to see what’s what with the meter. +/- 0.1 is well within its bounds of degrees of freedom. And no, I don’t ever recall measuring a 0.0.
But eating a full (real) pizza seems like a pretty drastic way of performing n=1 tests. Hopefully calibrating your Mojo wasn’t the reason you gorged. 
One of the reasons ketone production is high in the beginning of a ketogenic diet is that the skeletal muscles have to limp along on ketones for a while, before they recover their ability to metabolise fatty acids. Once they are healthy enough to metabolise fats effectively, they actually prefer the fats to ketones (which are partially-metabolised fats), and the liver then doesn’t need to produce so much acetoacetate, acetone, and β-hydroxybutyrate.
In the absence of dietary glucose, the brain does well on ketone bodies, since fatty acids are too large to cross the blood-brain barrier. The brain uses ketones not only as fuel, but as raw materials for cholesterol production. The brain is made of a large amount of cholesterol, and it is essential for the transmission of nerve impulses, which is why the body never entirely stops making ketones, even on a high-glucose (carbohydrate) diet.
A low-carbohydrate diet is called “ketogenic” because the detection of β-hydroxybutyrate in the blood stream is a reliable indicator that serum insulin has dropped sufficiently to put the body into a healthier metabolic state. But we should really be referring to and thinking of it as a “low-insulin” diet. We also focus on the ketone bodies as fuels, but they also have powerful epigenetic effects, which are probably almost as important, or perhaps more so. B-hydroxybutyrate stimulates the production of endogenous defences against oxidative stress, and acetone has powerful beneficial epigenetic effects on brain function, just to name two examples.
Excellent explanation @PaulL as usual. I wonder though…
… Would calling it a “more stable-insulin” diet be more on point?
I’d think that excursions from baseline insulin levels should be markedly reduced though carb-restriction in conjunction with greater tissue sensitivity to insulin - which is what the reversal of metabolic syndrome/T2D achieves. 
I personally wouldn’t use that term. My view is that the point of this way of eating is to keep serum insulin below a certain threshold, shown by Ralph DeFronzo and his team to be just under 25 μU/mL Above that threshold, the body is in glucose-metabolising, fat-storing mode; below it, in fat-metabolising, ketogenic mode. The two states are regulated by the relative proportions of glucagon and insulin.
But can insulin perform its essential functions if it never exceeds 25uu/mL?
As the body’s primary anabolic hormone, insulin needs to cycle above certain levels even in an insulin-sensitive individual in order to maintain healthy levels of body fat, muscle function, and other vital metabolic cycles… So is maintaining insulin beneath DeFronzo’s stated level sufficient to support these functions?
From a different perspective: What are target insulin levels for Type 1 Diabetics, i.e., who cannot naturally produce insulin on their own?
Absolutely. It’s a very powerful hormone, and when we’re not insulin resistant, cells are exquisitely sensitive to insulin signaling. Look at it this way: for two million years, before people started eating a lot of carbohydrate, they didn’t starve to death when they had food to eat, not unless they were Type I diabetics. And we know that a low-carbohydrate, high-fat diet can help Type I diabetics, as was shown back a century ago, before insulin was discovered.
So we evolved with low insulin levels, which is one of the reasons that hyperinsulinaemia has such a pernicious effect on the body.
They are altogether too high, in standard treatment, because the logic runs thus: People can’t stop eating carbohydrate, so we might as well give them more insulin so they can eat all the sugar they want. However, that way lies blindness, amputations, and cardiovascular disease.
Dr. Richard Bernstein finds that a low-carbohydrate, high-fat diet eliminates the need for bolus doses of insulin before meals (because the patient doesn’t need to worry about covering a high carbohydrate intake with insulin) and also lets patients reduce their daily dose somewhat, as well. LCHF also allows Type I diabetics not to worry about hypoglycaemic episodes, because they are mostly caused by overdosing on insulin.
Taubes makes the point that hypoglycaemia did not exist as a medical condition until the advent of insulin treatments in 1923. Bernstein developed a principle he calls the “law of small doses,” meaning that when quantities of carbohydrate and hence insulin are low, there is much more room for correcting any dosing errors with very little risk of disaster. It’s when carb intake is high and the patient tries to cover it with bolus insulin that the insulin level swings between hyper- and hypo- levels.
@PaulL Okay, I’m sold.
FWIW, as an individual who has never (knowingly) had his insulin level tested, I’ve got no idea what mine is, has been, or will be.
They won’t test it, because there’s no drug they can give you, and no one can make a profit by telling you to knock off the sugar, starches, and grains.
Probably so, but since I order my own tests there’s no one to blame for my lack of insulin testing other than myself. This is a case of n=0.
It was a small pizza, and I ate everything but two slices. I will eat things like ice cream and pizza periodically. These were my downfall, as they got me fat, but I still like to eat them periodically.
And, yes, after trying multiple tests with ketones, I realized that (1) the measurements are terrible (I have a picture of 3 meters showing 0.2, 0.4 and 0.8 mmol/l, all from the same time); and (2) eating more fat (or more protein) had no apparent relationship with ketones (possibly because of (1)).
I just wanted to see whether I could ever “get kicked out” of “ketosis”.
Here are my “fasting” (maybe only 8 hours, maybe 12) insulin levels. The latest 2 I think are caused by a new drug, which has raised my glucose (HbA1c went from 5.2 to 5.6) and c-peptide too.
Ah, I’d read in your initial post that you ate an entire pizza - with no mention of size or any leftovers.
Finish those last two slices and then remeasure
