Noob


(William) #1

I’m new here and new to keto. I’ve done IF 16:8 for years - just find it simple. But my waistline has increased and I’m determined to sort it out. Keto an IF appear to compliment each other quite well. So anyway, I’ve done my 1st month and lost 12lbs. I ended up a piece of cake in Xmas day, but still showed ketones in urine the next day… so I thought I got away with. However, today (2 days later) my ketones have gone for the first time in month. Did the cake replace my glycogen store and I’m now burning back through that b4 getting back into ketosis.


#2

First, forget ketones exist. They don’t matter as far as you babysitting them. Ketone levels don’t correlate with the speed of fat loss so watching them is pointless. Eat correctly 90% of the time and you’ll be good.

Yes, once you eat carbs (even the good ones) aside from what you’re burning right then as fuel your liver will start reloading. You’ll still show ketones in your blood until you burn them but then you’re back on liver glycogen until that’s depleted. If you ate enough to fill your liver up then your muscles start reloading their glycogen stores. It’s not a bad thing. The scale will show weight but it doesn’t matter since it’s not fat. Once your liver burns off what It’s got you’ll start making ketones again. Not a big deal at all.

There’s always a 2-3 day lag when you start reloading so ignore it all, weigh if you want so you can watch the trend but take it in context.


(A fool and his bacon are soon parted) #3

More likely the cake elevated your insulin high enough to inhibit ketogenesis. Once your serum glucose drops low enough for the insulin to drop as well, then your liver will start producing ketones again.


(William) #4

Thanks for taking the time to reply. I get that urine ketone levels are kind of irrelevant, but surely they are in indication that you’re in ketosis


(Edith) #5

Urine ketone levels are mostly indicative of wasted ketones. Once your body can use its new fuel source efficiently, there is less waste, and therefore, little to no ketones will appear in your urine.

As I am typing this, I realized that is why the urine test strips are good for type one diabetics and people who don’t control their type 2 diabetes with keto: ketoacidosis creates an overabundance of ketones that will be urinated out no matter if you are using some of them for fuel. If you are in nutritional ketosis, once adapted, you are using up what you make and are therefore in balance. No waste ketones to be excreted.


(Michael - When reality fails to meet expectations, the problem is not reality.) #6



49%20AM


(Michael - When reality fails to meet expectations, the problem is not reality.) #7

Somewhat related, but further afield and possibly of greater interest for the technically minded:

23%20AM

In Brief

An integrated response driven by leptin levels plays an important role during starvation to promote the shift from carbohydrate to fat metabolism and in maintenance of gluconeogenesis

Highlights

  • Hypoleptinemia promotes HPA-axis-driven WAT lipolysis to maintain euglycemia
  • Increased hepatic acetyl-CoA content maintains euglycemia during starvation
  • Substrate limitation reduces mitochondrial VCS and VPC flux during a prolonged fast

SUMMARY

The transition from the fed to the fasted state necessitates a shift from carbohydrate to fat metabolism that is thought to be mostly orchestrated by reductions in plasma insulin concentrations. Here, we show in awake rats that insulinopenia per se does not cause this transition but that both hypoleptinemia and insulinopenia are necessary. Furthermore, we show that hypoleptinemia mediates a glucose-fatty acid cycle through activation of the hypothalamic-pituitary-adrenal axis, resulting in increased white adipose tissue (WAT) lipolysis rates and increased hepatic acetyl-coenzyme A (CoA) content, which are essential to maintain gluconeogenesis during starvation. We also show that in prolonged starvation, substrate limitation due to reduced rates of glucose-alanine cycling lowers rates of hepatic mitochondrial anaplerosis, oxidation, and gluconeogenesis. Taken together, these data identify a leptin-mediated glucose-fatty acid cycle that integrates responses of the muscle, WAT, and liver to promote a shift from carbohydrate to fat oxidation and maintain glucose homeostasis during starvation.

@PaulL I think you will find this study of the mechanics of ketogenesis very interesting.

…The shift from glucose metabolism to fat and ketone metabolism is thought to be primarily orchestrated by a decrease in plasma insulin concentrations and, to a lesser extent, an increase in plasma glucagon concentrations…

…the effect of starvation-induced hypoleptinemia on glucose and fat metabolism has not been conclusively demonstrated. In this regard, we hypothesized that hypoleptinemia may be a critical signal to increase white adipose tissue (WAT) lipolysis through activation of the hypothalamic-pituitary-adrenal (HPA) axis, resulting in increased hepatic acetyl-CoA content and pyruvate carboxylase activity, thereby maintaining glucose homeostasis and increasing hepatic ketogenesis during starvation.

DISCUSSION

To prolong survival during an extended fast, mammals must shift from a primary reliance upon carbohydrate metabolism to a primary reliance upon fat and ketone metabolism in order to maintain adequate substrate supply to the brain, heart, and other organs, thus preserving essential protein stores that would otherwise be catabolized to support gluconeogenesis (Cahill, 1970). While insulin and, to a lesser extent, glucagon have long been thought to be the major orchestrators of this transition from glucose to fat/ketone metabolism, here, we demonstrate a leptin-mediated glucose-fatty acid cycle that is essential to support this process…

PS: To prevent side-tracking this topic, I created a new topic here to discuss this study.


Leptin in Initiation and Maintainance of Ketosis