Wed, Oct-17-12, 17:35
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Senior Member
Posts: 6,498
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Plan: VLC, mostly meat
Stats: 202/200/165
BF:
Progress: 5%
Location: Montreal, Quebec, Canada
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Quote:
Originally Posted by OregonRose
I dunno, Martin. I think targeting ketone levels/insulin inhibition makes sense. Speaking as someone who's eaten zero-carb for three years (meat, butter & eggs, with very infrequent, and very minor, deviations), I was quite surprised to get an "undetectable" blood ketone reading on my BG meter ketone strips. Ketosis may turn out to hinge on more than simply LC compliance -- it'd be damn hard to find anyone more "compliant" than a ZCer like me.
There could be variations in gluconeogenesis, for instance, or, as I suspect, insulin hypersecretion that is NOT the simple result of diet-induced insulin resistance, but is perhaps familial. I suspect this because of my frightening family history of cancer (nearly everyone's had it, and those who've died, died with/of it).
So from my perspective, I'm glad Fine et al are targeting a biological mechanism. For some people, compliance with a general LC, or even VLC -- or even ZC, for crying out loud -- may not be enough to achieve a sufficient level of blood ketones, which seems to be the key variable corresponding to cancer growth inhibition.
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Well, I think we agree here. There's several things going on from what I can see. First, relying on urine ketones to see how much fat you eat is like relying on urine glucose to see how much carbs you eat. But then again, if you can't detect some ketones then obviously something else is going because with ZC, we should detect a consistent amount of ketones in urine even when everything is working as it should. This expectation comes from the Bellevue all-meat trial results of course. It could just be that the detection tool is just not sensitive enough. Or, like you say and like I pointed out in my comments on Richard's blog, it could be something more serious and significant.
Like I said in one of my comments, if it is something else, then we must look at that. Sure, we can target insulin inhibition directly for the time being, but then what? What if the thing that is responsible for the disorder in insulin signaling is also responsible for cancer independently of insulin signaling? Even if it's not, then a targeted therapy will only be effective as long as we keep it up.
Richard and Eugine both said they're looking at a very specific thing - insulin inhibition and ketosis - and they acknowledge that it's not all that simple, even considering the conclusions they draw from that study.
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