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Old 06-23-2007, 03:44 PM   #3
fullofbeans
Senior Member
 
Join Date: Jan 2007
Location: UK
Posts: 617
Thanks for your answer Becki, but I am afraid I have to disagree;

Glucose is regarded as the preferred energy source for all cells in the body with ketosis (fat burning) being regarded as a crisis reaction of the body to a lack of carbohydrates in the diet.

Glucose is be used by all cells but in order to burn fat you need to enter the krebs cycle (aerobic process). Most cancer cells only uses anaerobic processes (Glycolysis).

Once glycogen store have been used up after about 48 hours, the adult brain starts burning ketones in order to more directly utilize the energy from the fat stores that are being depended upon, and to reserve the glucose only for its absolute needs, thus avoiding the depletion of the body's protein store in the muscles.

Alaska Angel posted about this trial a while ago, where they put people on an Atkins diet (kind of), so I would not be so quick at dismissing whole idea if they have bothered studying this idea:
http://www.clinicaltrials.gov/ct/gui...4054?order=100

This kind of diet high fats and proteins medically can be referred to as ketogenic diet as the effect of reproducing body under fasting condition. Please at this point fasting (use of fatty reserves) must not be confused with starvation.

Secondly Anaerobic pathways (without oxygen) yield 2 ATP’s per unit of glucose. This is the type of pathway that most cancers utilise. Aerobic pathways (with oxygen) yield 32 ATP’s, a much more efficient system. Normal cells utilise the aerobic pathways, therefore in period of low blood sugar your normal body cells should survive much much longer than abnormal cells.

Other benefit of fasting includes regeneration of organs such as liver through rest, increase of immune system (80% usually used in digestive purpose).
I think have just convinced myself..:-)
__________________

35 y/o
June 06: BC stage I
Grade 3; ER/PR neg
Her-2+++; lumpectomies

Aug 06: Stage IV
liver mets: 6 tumours
July 06 to Jan 07: 2*FEC+6*Taxotere; 3*TACE; LITT
March 07- Sept 07: Vaccination trial (phase 2, peptide based) at the UW (Seattle).
Herceptin since 2006
NED til Oct 09
Recurrence Oct 2009: to internal mammary gland since October 2009 missed on Oct and March 2010 scan.. palpable nodes in May 2010 when I realised..
Nov 2011:7 mets to lungs progressing fast failed hercp/tykerb/xeloda combo..

superior vena cava blocked: stent but face remains puffy

April 2012: Teresa Trial, randomised to TDM1
Nov 2012 progressing on TDM1
Dec 2012 blockage of my airways by tumours, obliteration of these blocking tumours breathing better but hoping for more- at mo too many tumours to count in the lungs and nodes.

Dec 2012 Starting new trial S-222611 phase 1b dual egfr her2+ inhibitor.



'Under no circumstances should you lose hope..' Dalai Lama
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