A new book, The Fat Switch, was recently released. It is a timely book. As you may know, the number of overweight people in our country has grown to the point that today, more than two-thirds of us fall into that category. We’re now entering the holiday season when weight gain sneaks up on us, so this is a good time to learn about the fat switch.
The author, Richard Johnson, MD, is superbly qualified to write this book. He is a practicing physician and scientist who is Professor of Medicine at the University of Colorado in Denver. His research over the past quarter century has focused on the kidneys and hypertension as well as on the impact of sugar and fat metabolism on health.
Dr. Johnson majored in anthropology before going into medicine, so he brings a broad evolutionary perspective to his research in the microscopic cellular world. Perhaps this fusion between macro and micro worlds enabled him to see connections that led him to his theory of the “Fat Switch.”
His observations about fat storage in animals that hibernate and birds that migrate incredibly long distances led him to wonder if there was a fat switch that could be turned “on” and “off” in these animals, and more specifically, if there is a fat switch of some kind involved in human obesity. His book is a delight to read as he deftly interweaves animal and prehistoric human stories with his scientific narrative about human physiology today.
As it turned out, Dr. Johnson and his lab found evidence of an intracellular “fat switch” in humans. His book describes the discovery of this switch and how it works. I won’t go into all the technical details involved in delineating the “fat switch,” but it’s worth summarizing briefly to grasp the underlying concepts entailed.
Mitochondria are sub-microscopic units in every cell that are responsible for generating the energy needed by the cell and the body. The mitochondria manufacture a chemical called adenosine triphosphate (ATP) which drives chemical reactions in the cell by giving up one or two of its phosphate groups. This donation of phosphate groups is the source of energy for the cell. It is the same process that provides energy for all forms of life.
Uric acid is a by-product of ATP and various nucleic acids like RNA and DNA. We’ve known for a long time that uric acid is a waste product that causes gouty arthritis. In the last few decades, Dr. Johnson’s lab and other labs have shown that high uric acid levels are a factor in causing high blood pressure. Now, these scientists have discovered that uric acid is also involved in regulating fat metabolism.
Intracellular uric acid puts stress on the mitochondria, injuring some of the enzymes needed for energy production. The net result is that energy manufacture is decreased or diverted to fat instead of producing more ATP needed for continued energy production. As a result, food energy is converted preferentially into fat instead of being used up as energy.
What causes rising uric acid levels in our body’s cells? Fructose provides the surprising linkage here as it turns out to be the master driver of the fat switch. Fructokinase, the main enzyme used to process fructose in the cell, consumes ATP like crazy in this process, turning it into a form of AMP (adenosine monophosphate) that eventually breaks down into uric acid. Rising uric acid levels then stimulate increased fat accumulation and storage.
Fructose acts in other ways to promote fat storage. In addition to raising serum triglycerides and causing insulin resistance, it paradoxically stimulates increased food intake. Leptin is a hormone released by fat cells to let the brain know it’s time to quit eating. Glucose stimulates the release of leptin, but fructose does not, so high fructose intake does not inhibit overall food intake as it should. The signal to quit or slow down doesn’t work with fructose!
Dr. Johnson’s detective work in unraveling the roles that fructose plays in driving obesity is brilliant. As always in science, it is likely to take several years for other scientists to confirm Dr. Johnson’s work, so it may be years before the key role of fructose in our obesity epidemic is widely accepted. My own view is that we know enough now to be proactive for our own health.
What does this mean in practical terms? As usual, prevention is easier than correction. Minimizing fructose is most important to help prevent obesity and its complications. Since sugar is half fructose, and since high fructose corn syrup (HFCS) is found in many commercial food products, it make good sense to minimize sweets and commercial products that contain HFCS.
Fruit contains fructose, but in lower concentrations than is true for most commercially sweetened foods. In addition, fructose in fruit is found in the context of abundant fiber and antioxidants that buffer and protect us from its adverse effects. Much research shows that most fruit is not only safe, but is good for health. It’s when fructose is consumed as an extract, as it is in sugar and sugar-sweetened foods, that it can cause serious health consequences.
What about Thanksgiving and Christmas dinners? Does this mean that one must skip these festive occasions? Not at all. Please enjoy them. Most of the food prepared for these meals is good, healthy food. Sampling a few of the sweet desserts is even OK. Just don’t go overboard on the sweets. Happy Holidays!
Ed Dodge, MD, MPH
This post was published first in Dr. Ed Dodge’s Wellness Newsletter, Nov. 17, 2012 • Volume IV, No. 11.