Wink Health: Making Five Guys Less Fattening

You start by questioning the background and motives of my colleagues. While I have thoughts on how to respond to this, I choose to stick to discussing the facts.

Then you represent the goal of my experiment in the following way: “can I stuff enough kale in my mouth to slow down the release of insulin, and therefore reduce glucose.” This is not accurate. My goal was to see if I could influence my digestive system to release glucose into the blood more gradually so as to minimize insulin signaling to fat cells. More explicitly, the amount of glucose is about the same in the two meals; it was the amount of insulin signaling by my body that changed.

I will add additional detail that I do not mention in my blog post. Cells that have high need for glucose do not need much insulin signaling. In response to their need, they already have placed more glucose transporters on their cell membrane. Gratuitous insulin signaling causes fat cells to absorb glucose that could have been absorbed by a high-need muscle cell.

Then you say, “Here’s a few other things that reducing insulin does....” From your wording, particularly in your use of “other,” you seem to agree that less insulin signaling means less fat cell growth and that your concern is primarily with its “side effects.” I will address amino acids and potassium in a later post. For now, I will address your point about brain signaling.

Actually, too much insulin signaling interferes with leptin signaling, making you respond less to leptin signaling. Leptin is the satiety hormone that is released by your fat cells. The neurons in your hypothalamus that have receptors for insulin also have receptors for leptin, and unfortunately for us, they have commonalities in their signal transduction pathways. So a lot of insulin signaling interferes with leptin signaling. This makes leptin signaling less effective and makes you want to eat more in spite of having enough body fat. (See the paper, “The First Law of Thermodynamics Revisited” by Robert Lustig of UCSF.)

You state firmly, “Fear not glucose and insulin. Fear insulin resistance and glucose intolerance.” You do not state however how you would advise someone to avoid insulin resistance and glucose intolerance. My view is that slowing down the digestion rate of your meals, such as I have done here, is part of the strategy for doing so.

Unfortunately, I have to run now, but I will address your remaining points later. I am also happy to write another blog post with ample references to primary research literature.

"Oversimplified models of biochemistry" - when insulin binds to an insulin receptor on a fat cell, the fat cell activates LPL, translocates GLUT4 to the cell membrane, and inhibits HSL. What else am I missing?

"No measure of insulin" -- insulin is not as easy to measure using off-the-shelf devices. If one meal leads to higher blood glucose levels than another, especially if it is vastly higher, it is a reasonable working assumption that it elicits a greater insulin response.

"No control of meal time" -- both meals were dinners.

"No control of fasting time" -- I ate the same amount during the day prior to each meal. Activity levels were also similar.

Re: widely varying blood glucose levels, in my own experience, it is very rare to see a meal cause a blood glucose concentration reach 150 mg/dL. This is very, very high amongst my meals and only happens with meals like this.

The following meal would most certainly be nowhere near 150 mg/dL no matter the time of day: vegetables (kale, broccoli, cauliflower), black beans, sardines, and avocado.