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My comments in answer to Jonny Bowden’s Huffington Post take on the sugar tax where he suggested that despite it’s flaws, “it’s all we’ve got.” I insisted that It’s not all we’ve got. We have the science and, in one afternoon, Bloomberg could convene a panel of scientists to evaluate presentations by all the players including me who believe that sugar is a smokescreen for not facing the importance of total carbohydrate restriction which you [Jonny Bowden], among others, have explained. Everybody should be heard. What I see is another rush to judgement like the low fat fiasco which we still have with us.

That you “have to do something” comes right out of Senator McGovern’s mouth as in Fat Head. And “deadly white substance that literally creates hormonal havoc and appetite dysregulation … promoting metabolic syndrome, diabetes, obesity and heart disease” is way outside of the bounds of science. I am not the only one to point out that Lustig’s population study represented the return of Ancel Keys.

We go with science or we don’t.

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Everybody has their favorite example of how averages don’t really tell you what you want to know or how they are inappropriate for some situations. Most of these are funny because they apply averages to cases where single events are important. I’ll list a couple in the text boxes in this post. From the title:

If Bill Gates walks into a bar, on average, everybody in the bar is a millionaire.

Technically speaking, averages start with the assumption that deviations are due to random error, that is, that there is a kind of “true” value if we could only control things well — if there were no wind resistance and all balls were absolutely uniform, they would always fall in the same place; any spread in values is random rather than systematic.
Standard_deviation_diagram.svg
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The reporter from Men’s Health asked me: “You finish dinner, even a satisfying low-carb dinner,” — he is a low-carb person himself — “you are sure you ate enough but you are still hungry. What do you do?”  I gave him good advice. “Think of a perfectly broiled steak or steamed lobster with butter, some high protein, relatively high fat meal that you usually like.  If that doesn’t sound good, you are not hungry.  You may want to keep eating. You may want something sweet.  You may want to feel something rolling around in your mouth, but you are not hungry.  Find something else to do — push-ups are good.  If the steak does sound good, you may want to eat. Practically speaking, it’s a good idea to keep hard-boiled eggs, cans of tuna fish around (and, of course, not keep cookies in the house).” I think this is good practical advice. It comes from the satiating effects of protein food sources, or perhaps the non-satiating, or reinforcing effect of carbohydrate. But the more general question is: What is hunger? Read the rest of this entry »

Guest post: Dr. Eugene J. Fine

Last time I discussed our pilot study showing the effects of carbohydrate (CHO) restriction & insulin inhibition (INSINH) in patients with advanced cancers.  We described how the molecular effects of INSINH plus systemic (total body) effects like ketosis might inhibit cancer growth. My goal now is to present the underlying hypothesis behind the idea with the goal of understanding how patients with cancers might respond if we inhibited insulin’s actions? Should all patients respond? If not, why not? Might some patients get worse? These ideas were described briefly in our publication describing our pilot protocol. Read the rest of this entry »

Dr. Eugene J. Fine.   Dr. Feinman invited me to contribute a guest blog on our recently published cancer research study: “Targeting insulin inhibition as a metabolic therapy in advanced cancer: A pilot safety and feasibility dietary trial in 10 patients” which has now appeared in the October issue of the Elsevier journal Nutrition, with an accompanying editorial.  Today’s post will focus on this dietary study, and its relation to the general problem of cancer and insulin inhibition. Part II, next week, will discuss in more detail, the hypothesis behind this study. Richard has already mentioned some of the important findings, but I will review them since the context of the study may shed additional light. Read the rest of this entry »

In the last post, I had proclaimed a victory for dietary carbohydrate restriction or, more precisely, recognition of its explicit connection with cell signaling. I had anointed the BMC Washington meeting as the historic site for this grand synthesis. It may have been a matter of perception — many researchers in carbohydrate restriction entered the field precisely because it came from the basic biochemistry where the idea was that the key player was the hormone insulin and glucose was the major stimulus for pancreatic secretion of insulin. We had largely ignored the hook-up with cell-biology because of the emphasis on calorie restriction, and it may have only needed getting everybody in the same room to see that the role of insulin in cancer was not separate from its role in carbohydrate restriction. Read the rest of this entry »

It was in July of 2012 that I suddenly realized that we had won, at least scientifically. It was now clear that we had a consistent set of scientific ideas that supported the importance of insulin signaling in basic biochemistry and cell biology and that there was a continuum with the role of dietary carbohydrate restriction in obesity, diabetes or for general health.  The practical considerations, how much to eat of this, how much to eat of that, were still problematical but now we had the kernel of a scientific principle. In fact, it was not so much that we had the answer as that we had the right question.  In science, the question is frequently more important than the answer.  Of course, winning wasn’t the original idea. When my colleagues and I got into this, about ten years ago, coming from basic biochemistry, we hadn’t anticipated that it would be such a battle, that there would be so much resistance to what we thought was normal scientific practice.

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