Hi all. I am on day 6 and have noticed that for the past 4 days or so, my ketostix have progressed as expected from tan->light pink-> mauve-> purple-> maroon. I know the use of Ketosis is controversial, especially as people become far adapted, but so far the outcomes I’ve gotten have been as expected.
My question is, are the extra ketones I’m seeing in my urine necessarily coming predominantly from my liver stores ( via beta oxidation of FAs)? I’m eating a lot of fat (to satiety) and wonder if I could be eating so much fat that I’m making surplus acetyl CoA which is then undergoing ketogenesis. It’s been a while since I took biochemistry, so hopefully this isn’t an absurd question.
Also, I’d really like to better understand what happens to all of the fat we consume when eating this way, since, to the best of my understanding, it doesn’t just get stored. Anyone know of any studies that followed consumed fat with some sort of tracer while body was predominantly using Ketosis for energy?
daddyoh
(Eric - The patient needs to be patient!)
#2
Yes from burning fat stores or using the fat in the liver we eat. Some people will stop producing excess ketones once fat adapted (unless fasting). The strips turn colors for me even though I’m 6 months in and clearly fat adapted.
Ketones are produced in the liver. The readings you get from your urine are unused ketones.
Most of the time, these tests detect acetone, and occasionally acetoacetic. The presence of both is a sure sign you are in ketosis. Beta-hydroxybutyrate, which is the most biologically active of the ketones, is largely present in blood and, unfortunately, ketone strips won’t detect it.
The thing with fat is, it’s difficult to overeat it if we eat to satiety. Therefore this shouldn’t be an issue with a proper ketogenic diet. Here’s an interesting thread on this very issue. There’s some interesting info posted regarding Dr. Jason Fung and some thoughts from his book, the Obesity Code (I think).
In a metabolically healthy person, eating excess fat will cause the metabolism to speed up. Healthy leptin signaling will cause the increase in metabolism as the body won’t want to store excess fat, and will be forced to speed up and utilize it. This seems like a great way to speed up metabolism. I imagine it works best to push your metabolism into overdrive by eating all this fat in low frequency, as a slow fat drip wouldn’t have the same speeding effect.
The problem is if an obese person with improper insulin and leptin signaling eats too much fat, it won’t speed metabolism and could lead to weight gain. Seems like the goal in that individual is to reduce insulin as much as possible, which of course is the goal of keto.
This doesn’t sound right, sorry. Phinney and Volek define nutritional ketosis as a serum β-hydroxybutyrate level of 0.5 mg/dL or higher. Every relevant post I’ve read on these forums seems to take it for granted that what people are measuring in their blood is β-hydroxybutyrate. The way it was explained to me is that the urine strips test for acetoacetate, the breath analyzers for acetone, and the blood meters for β-hydroxybutyrate. I was under the impression that the same meter is usually capable of testing for either glucose or β-hydroxybutyrate, depending on which strip one uses. Dr. Phinney certainly gives the impression that the blood meters can do this.
Forgive me, but again, this isn’t quite the way I have seen it explained (source: Robert H. Lustig, The Hacking of the American Mind). There are two satiety hormones, peptide YY, which is secreted by the stomach as it expands, and leptin, which is secreted by the adipose tissue after a certain amount of triglycerides has been stored. Both work to suppress appetite, but the former signals a full stomach, the lattter, the presence of sufficient stored energy. I believe that the speeding of the metabolic rate is achieved by a different mechanism.
Certainly the production of ketone bodies is rate-limited by the amount of available acetyl CoA, and by the serum insulin level. The intake of carbohydrate and the consequent serum glucose and insulin levels make a difference. In the context of an abundance of carbohydrate, the high insulin level signals the liver to turn the glucose into triglycerides, and the resulting drop in acetyl CoA inhibits ketogenesis. In the absence of glucose and insulin, the process of lipolysis creates enough acetyl CoA for ketogenisis. The insulin/glucagon ratio is also relevant and is determined by the level of carbohydrate/glucose. As Bikman explains, in the context of low carbohydrate, an increase in insulin (resulting from, say high protein intake) is matched by an equivalent increase in glucagon, which keeps the i/g ratio the same; whereas ingesting a quantity of carbohydrate stimulates insulin without an equivalent glucagon release, so the i/g ratio increases dramatically.
Thanks @PaulL The second quote I posted seemed a little too good to be true. OD on fat and you zoom around all over the place. I can’t say I wasn’t intrigued because the person attributed Fung as saying it.
It’s true that, given abundant energy, the body can increase the basal metabolic rate, but it’s more complicated than your source made it sound. It’s entirely possible something got garbled in transmission. Benjamin Bikman talks a lot about mitochondrial “decoupling” in the adipose tissue, which is basically that, in the absence of insulin the mitochondria in fat cells can metabolize quite a bit of fat in excess of the metabolic needs of the cell, thus wasting a noticeable amount of energy. And this is only one of the ways that keto helps the body increase its energy expenditure. I never realized, when I first got into this way of eating, just how fascinating the body’s mechanisms can be!
