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Gaining Weight on Keto? Keto Plateau Science | 5 Keto Fixes for Better Results- Thomas DeLauer…
1) Overdoing the Fats:
bHB is a ligand for certain receptors in the body – it binds to receptors on the surfaces of cells and activates processes within those cells as a result (similar to how neurotransmitters and hormones work)
bHB can activate hydroxycarboxylic Acid Receptor 2 (HCAR2), a Protein Coding gene – among its related pathways are Peptide ligand-binding receptors and cAMP signaling pathway.
HCAR2 activation by bHB (or other ligands) reduces lipolysis in adipocytes – for bHB, this might represent a feedback mechanism to regulate availability of the fatty acid precursors of ketone body metabolism.
By doing this, ketones can actually regulate their own production through negative feedback – elevated levels of ketone bodies slow down the rate at which lipid is removed from fat cells, likely so that this fatty acid release doesn’t spiral out of control.
**Subset of people that greatly increase their fat intake and they think it’ll speed up the fat burning processes, not knowing that fatty acid release is regulated**
2) Crossing the carb barrier (knocking out of keto but still having the fats):
Knocking yourself out lends itself poorly in a couple ways: for one, you’re in a gray area in terms of energy as you’re not low enough on carbs to be producing ketones and not high enough on carbs to be receiving enough energy from them.
3) Mixing Fats and Carbs (accidentally)
Acylation stimulating protein (ASP) is induced by fat and both ASP and insulin stimulate the secretion of each other.
So, in an indirect way, fat does stimulate insulin & insulin stimulates a fat storing helper ASP.
Another storing hormone is a gut produced signaling molecule called glucose-dependent insulinotropic peptide (GIP.)
GIP is induced by both carbs & fat and to a much lesser extent, protein and fiber – GIP has its own fat storing action on LPL and causes more insulin to be released (here again fat can result in indirect insulin secretion.)
4) Improper Cheat Meal Protocol:
In a study published in the American Journal of Physiology, 22 young healthy subjects (11 men and 11 women) were given, in a randomized order, an isoenergetic meal [carbohydrate (81%) or fat (79%)] or remained fasting.
Leptin response was higher after the carbohydrate meal than after the fat meal and while fasting.
5) Focusing on Ketones Being High all the time:
Glucagon drives ketogenesis by reducing hepatic malonyl-CoA – Malonyl CoA inhibits fatty acids from associating with carnitine by regulating the enzyme carnitine acyltransferase, thereby preventing them from entering the mitochondria, where fatty acid oxidation and degradation occur.
The fall in malonyl-CoA concentration activates carnitine acyltransferase I such that long-chain fatty acids can be transported through the inner mitochondrial membrane to the enzymes of fatty acid oxidation and ketogenesis.
Food increases the liver concentration of malonyl-CoA, inhibits carnitine acyltransferase I and reverses the ketogenic process.
Acetyl-CoA carboxylase catalyzes the production of malonyl-CoA from acetyl-CoA. Malonyl-CoA reduces the activity of carnitine palmitoyltransferase I, an enzyme that brings fatty acids into the mitochondria for β-oxidation.