Thursday, March 21, 2013

Why cells go bad: a new appreciation and understanding of ATP opens up an untapped avenue for fighting diabetes, cancer, aging, etc.

It’s refreshing to see people beginning to think clearly and rationally and move away from gimmicky diets that have little basis in fact, reality, or objectivity, and to ones that are firmly seated in all aspects of human physiology and science.

After all, this is why most of us choose to eat a certain way, that is to be as healthy as we can be, both physically and mentally . . . not to, say, replicate how our caveman ancestors supposedly ate and lived.

It’s due to this line of reasoning that carbohydrates, and especially sugar and fructose, have fallen by the wayside of late, driven by an irrational fear, bordering on obsessiveness, that’s evolved to where sugar is now conceived of as a toxic poison and blamed for causing diabetes, cancer, obesity, gout, etc. (Thank you Dr. Lustig.)

It’s important to point out that sugar is used by virtually every cell in the body to generate energy, or ATP.  The brain is especially reliant on glucose for optimal functioning: The brain represents only 2 percent of the body’s total weight yet accounts for 15 percent of the body’s total energy expenditure. 1 Indeed, the brain is a voracious sugar guzzler, and sugar, not ketone bodies, is its preferred fuel source, despite popular discourse to the contrary.  Insulin and sugar make us smarter 2 so it stands to reason that ketosis has the opposite effect.

Friday, March 8, 2013

Diabetes, Dangerous Fat, and Protective Sugar

Since the discovery of the so-called “glucose-fatty acid cycle” in 1963, there has been more and more evidence accumulating linking free fatty acids with diabetes (Randle, Garland, Hales, & Newsholme, 1963).  Briefly, the glucose-fatty acid cycle describes a competition, whereby the use of glucose becomes impaired by the presence of fatty acids and, to a lesser extent, vice versa (Cook, King, & Veech, 1978). 

Others had hinted at this fatty acid-induced blocking effect of sorts before.  Among them, was a guy named Apollinaire Bouchardat, a French pharmacist, who gave his diabetic patients sweet fruit and bread made from gluten, and had good results.  Others had applied Bouchardat’s dietary prescription and achieved equally good success.  More recently, an English physician, William Budd, following on the heels of these pioneers, gave his diabetic patients around 8 ounces of sugar daily, with only the intent of slowing the cachexia that was characteristic of long-standing poorly controlled diabetes.  Not only did most of his patients stop wasting away, but they also began to stop losing sugar in their urine when given this “saccharine treatment” (Hughes, 1862).

Another prominent clinician-researcher, Harold Himsworth, who was also first to show that insulin sensitivity in the tissues is reduced in diabetics, decades later, suggested, based on his clinical experiences and a review of the population data that high intakes of dietary fat (which raises free fatty acid levels) caused diabetes, and that diets rich in carbohydrates and low in fat were protective of it (Himsworth, 1934a, 1934b, 1936).

Friday, March 1, 2013

Insulin revisited, cell physiology, membrane pumps, and internet commenters

In my first “fact check” of Dr. Ray Peat, I had discussed the mechanisms by which insulin exerts its effects from the conventional textbook point-of-view.  I’ve gotten mostly good feedback on that post, and some idiotic ones, from the people who obviously didn’t take the time to read it, or if they did failed to understand it.  

Briefly, the conventional view is that insulin, upon being secreted by the β-cells of the pancreatic islets, acts on and activates the insulin receptors, initiating the insulin-signaling cascade.  This activation of the insulin receptor then provides a docking site for the insulin receptor substrate (IRS) proteins, which thereafter activate kinases in the vicinity that contain a specific SH2 domain, namely the kinase that phosphorylates the 3-position of the membrane lipid phosphatidylinositol 4,5-bisphosphate (PI 3,4 P2) to phosphatidylinositol 3,4,5-trisphosphate (PI 3,4,5 P3).

Figure 1 Insulin signaling pathways in the cell.
GLUT = glucose transporter (lower right)

This lipid product, PI 3,4,5 P3 thereafter activates the kinase, PDK1, and PDK1 phosphorylates and activates Akt, another kinase that moves throughout the cell’s cytoplasm, executing most of insulin’s actions, the most important of which for this post is the translocation of the glucose transporters from the cytoplasm to the plasma membrane.