Rob Hanna


Austin, Texas

University of Florida; New York University; The Rensselaerville Institute


Haven't created any projects yet! 

No lab notes posted yet!

Wow, sounds crazy difficult to grow human cells in vitro for testing. Makes me curious as to what might such cells be best established to test regarding the efficacy of dietary/nutritional ketogenic states on inhibiting cancer? I'm a layperson that's been in various stages of keto-adaptation for over two decades because I seasonally fast for lengthy periods. And tracked my ketones in urine, breath and blood–all seem to signal changes as I cycle through various stages of keto-adaptation, for example in deep fasts (10+ days) testing urine for acetoacetate first registers rises in ketone bodies and then eventual declines, purportedly because kidneys adapt and then conserve ketones instead of pumping them out to the waste stream. Meh, or so I've been told. As well, acetone exhaust from my lungs also seems to fluctuate (and/or my sampling, lol) during sustained ketosis. I believe breath acetone measures are proxy for beta-hydroxybutyrate circulation (BOHB) levels. If BOHB appears to be the crowning, culminating substrate (is it technically not a ketone?) that persists and becomes a steady fuel to nourish the brain (supposedly with minor amounts of glucose, ~30g/day, still in supply from liver gluconeogenesis) and skeletal muscles are then supposed to shift from using liver produced ketones into burning free fatty acids directly mobilized for energy, then this piques my curiosity and raises interesting questions about what exactly is inhibiting cancer when we're fully keto-adapted (or simply moving in that direction). Are we here testing: 1) presence of a sustained metabolic baseline amounts of BOHB on inhibiting cancer cells; and/or, 2) epigenetic and systemic metabolic effects of any type ketones on inhibiting cancer (as in does autophagy drive all cellular renewal, e.g. reversal of insulin resistance, plaque removal from arteries, etc. even to include cancer cells); and/or, 3) mechanically starving cancer cells from glucose (e.g. to apoptosis, or weakening them to other interventions such as chemo or radiation) because of some systemic level of ketones being used for energy; and/or, 4) something else? I'm just curious and very happy you guys are doing work in this field. Thanks for considering my comment. Cheers!
Sep 08, 2016
Part 2: Can low carbohydrate ketogenic diets inhibit cancers?
View comment