Wed, Mar-19-14, 12:33
|
|
Senior Member
Posts: 15,075
|
|
Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
|
|
Quote:
Originally Posted by 2thinchix
Is it really ketogenic, though? My understanding is that coconut oil, since it produces its own ketones when it breaks down, can make it APPEAR your body is in ketosis, even though it actually isn't. And 5 TBS a day is a LOT. Am I incorrect in my assumption?
|
There's an MCT-based diet for epilepsy, where they use MCT oil to allow the kids to eat more carbs and still remain in ketosis. I guess it depends--if the benefits come from ketones themselves, it might not matter where those ketones came from. To the extent that decreasing glucose metabolism matters--like say in cancer, I guess then probably it does matter. Mary Newport reported seeing improvements in her husband's Alzheimer's, originally, just stirring coconut oil into his oatmeal. Although she did go to a lower carb diet later on.
I'm wondering lately if increasing ketones through MCT oil would decrease gluconeogenesis--if gluconeogenesis occurs largely in response to the brain's demand for fuel, it makes sense that this might be true--making the true carb count of a fairly low carb diet effectively lower. There might also be a hormonal response to ketones of some sort that would alter the effect of glucose on the metabolism.
To the extent it's the ketones at work, though, I'd think lowest carbs possible plus coconut oil would be most effective.
http://www.ncbi.nlm.nih.gov/pubmed/24615175
Quote:
Abstract
Cancer cells express an abnormal metabolism characterized by increased glucose consumption due to genetic mutations and mitochondrial dysfunction. Previous studies indicate that unlike healthy tissues, cancer cells are unable to effectively utilize ketone bodies for energy. Furthermore, ketones inhibit the proliferation and viability of cultured tumor cells. As the Warburg effect is especially prominent in metastatic cells, we hypothesized that dietary ketone supplementation would inhibit metastatic cancer progression in vivo. Proliferation and viability were measured in the highly metastatic VM-M3 cells cultured in the presence and absence of β-hydroxybutyrate (βHB). Adult male inbred VM mice were implanted subcutaneously with firefly-luciferase tagged syngeneic VM-M3 cells. Mice were fed a standard diet supplemented with either 1,3-butanediol (BD) or a ketone ester (KE), which are metabolized to the ketone bodies β-hydroxybutyrate (βHB) and acetoacetate (AcAC). Tumor growth was monitored by in vivo bioluminescent imaging. Survival time, tumor growth rate, blood glucose, blood βHB, and body weight were measured throughout the survival study. Ketone supplementation decreased proliferation and viability of the VM-M3 cells grown in vitro, even in the presence of high glucose. Dietary ketone supplementation with BD and KE prolonged survival in VM-M3 mice with systemic metastatic cancer by 51% and 69%, respectively (p<0.05). Ketone administration elicited anti-cancer effects in vitro and in vivo independent of glucose levels or calorie restriction. The use of supplemental ketone precursors as a cancer treatment should be further investigated in animal models to determine potential for future clinical use.
|
|