Hi there. Relatively new to keto - have been doing “low carb” for a few months and looking to take the plunge and get into full ketosis, but I have a question about NOT being in ketosis. It is certainly possible to lose fat without being in ketosis - any non-keto weight loss involves losing fat. What is happening other than ketosis in this situation? For example, if I eat a low calorie / normal carb diet but I burn more calories than I take in each day, and I lose fat, was I actually in ketosis?
Burning Fat when NOT in Ketosis
amwassil
(Michael - When reality fails to meet expectations, the problem is not reality.)
#2
Ilana_Rose
(mole person)
#3
Yes. Whenever your body is burning fat for fuel ketones are being produced as a byproduct of fat metabolism. Most people are in mild ketosis every night while they sleep. What’s different about a ketogenic diet is that the aim is to stay in ketosis all the time by not eating the sorts of highly insulinogenic foods that prevent it. As your metabolism adapts to using fatty acids and ketones more effectively your hunger stabalizes and you can reap many other benefits.
carolT
#4
If you are not depleting your liver glycogen (which some healthy people can do overnight) you are using fat via beta oxidation as part of the Krebs cycle (TCA). Only when you switch to gluconeogenesis (GNG) as your source of blood glucose are you generating ketones. This can occur fasted or during prolonged exercise in most people. Eating carbs will shut down the process as glucose is supplied by food and liver glycogen is replenished
Detailed description:
In the liver, therefore, oxaloacetate is unavailable for condensation with acetyl-CoA when significant gluconeogenesis has been stimulated by low (or absent) insulin and high glucagon concentrations in the blood. Under these circumstances acetyl-CoA is diverted to the formation of acetoacetate and beta-hydroxybutyrate.
From Wikipedia
Ilana_Rose
(mole person)
#5
This is interesting. So why does the body use fat if there is still liver glycogen?
Screenack
(less is more, more or less)
#7
“Ketosis” is a metabolic process. Some of us (hello!) have never been able to show ketones on pee strips, and yet, my 44 waist is now 36, and I’ve dropped 65 pounds, and kept it off for years. If you keep your total carbs below 20 grams a day, you’ll be fine. You don’t have to “rig” anything.
Amy Burger argued that you can get into ketosis if you sufficiently calorie restrict, though that wasn’t the point she was making. Starving yourself on a high-carb, however, is a poor long-term dietary choice. If you want to lose weight quickly, that’s one thing. If you want to adopt a healthier way of eating, that’s another. Sugars and starches, evidence shows, is far more deleterious than commonly understood.
carolT
#8
The short answer is because there’s only a few hundred calories of liver glycogen available for energy, while fat availablity is close to unlimited unless insulin interferes with the process or you have a very low bodyfat %. You sjust can’t run everything purely on glycogen or you would collapse very quickly.
Your muscle mitochondria will use fat as a substrate when operating in non-glycolytic zones of exertion, and even the glucose dependent states are using fat simultaneously. Fat adaptation after being on a ketogenic diet will increase the amount of fat your muscles can use at a given exertion level. Constantly providing a source of glucose to avoid “the bonk” will never allow this adaptation to fully take place.
Fat can be used for energy production in the presence of liver glycogen without creating ketones as a by-product. Acetyl-CoA (produced from cleaving fatty acids) in excess of OAA supply will produce ketones and glucose. Acetyl-CoA can be used to produce energy without ketone production under normal circumstances (not keto) through beta oxidation.
The key to this whole process is insulin. In a T1D for example, there is no insulin (unless injected) and plenty of glucagon from the pancreatic alpha cells. This creates runaway lipolysis from fat cells (FFA) and the liver quickly switches into ketone and glucose production mode because OAA supply is overloaded and exhausted. Going unchecked this can lead to the dreaded ketoacidosis. Fasting or nutritional ketosis is simulating the same process by depleting the glycogen, turning on FFA release and GNG is depleting OAA. But it’s doing so in a controlled manner because of insulin-glucagon homeostasis of the functioning pancreas.
[also insulin promotes glycogen storage in the first place and inhibits the carnitine shuttle in mitochrondria]
The liver also uses fatty acids for cholesterol synthesis.
Fatty acids are enzymatically broken down in β-oxidation to form acetyl-CoA. Under normal conditions, acetyl-CoA is further oxidized by the citric acid cycle (TCA/Krebs cycle) and then by the mitochondrial electron transport chain to release energy.
WIKIpedia
atomicspacebunny
(Bunny)
#9
At least from what I gathered from C. Masterjohn, the less body fat (meaning very little: endomorph) you have when you do carb up the more likely the sugar is going to be stored in muscle and liver as glycogen; then the liver burns up (oxidizes) the rest not allowing insulin to store it as fat.
The more body fat you have (lots of it), the more likely that extra sugar your eating is going to be stored equally by insulin as body fat (after glycogen storage is replenished) but will also be stored in adipose tissue as glycogen (besides storing it as fat; individual homeostasis) but in very small amounts besides the muscle and liver. So it has to burn through that wall of glycogen also before it can get to the fat.
The fat is sitting over their in the corner saying “…hey you better give me some of that too because I might want to make myself bigger…” …lol
When fat cells get big enough or in number they start to act as a major endocrine organ sending instructions and demanding service from the liver as if it were a muscle tissue rather than the liver doing what it’s supposed to do when it does not have the extra clientele. Which ties in with what Nurse Cindy Miller was saying about your body not knowing it’s fat?
carolT
#10
There’s a whole bunch of subtypes for various glycogen storage disorders too. The most common one that isn’t genetic would be what you describe in some T2Ds where the liver has difficulty storing glycogen, maybe because of a fatty liver, and instead there is adipose glycogen generation.
[added link]
Note the process of tissue inflammation and endocrine (dys)function.
atomicspacebunny
(Bunny)
#11
…and look at their conclusion?
Conclusion: Our data establish glycogen mishandling in adipose tissue as a potential key feature of inflammatory-related metabolic stress in human obesity.
Ilana_Rose
(mole person)
#12
Thank you, @carolT. I always learn something from your posts. This was a definite missing piece for me.
carolT
#13
So, the million dollar question is…
What happens first, the inflammation or the IR?
There’s a theory out there that inflammatory substances (including alcohol, refined sugars, PUFAs etc) starting in the gut cause omental fat inflammation and the other effects in the liver, subcutaneous fat are downstream. But I’m not ready to do a wall of text about that today. 
atomicspacebunny
(Bunny)
#15
…and Dr. Michael Eades & Hyperlipid on hydrogenated vegetable oils and animal fats? (i.e. reverse electron transport and macrophage infiltration of adipose fat cells)