Newly-Discovered Hormone Produced By High-Fat, Low-Carb Diet 'Breaks Down Fat'
Posted Oct 01 2008 8:32pm
Drs. Maratos-Flier and Kliewer found the hormone behind Atkins diet
We have seen some truly remarkable research come out in favor of the Atkins low-carb diet this year, most notably the Stanford JAMA study from March 2007 showing it as the superior diet for weight and health.
But now we read in this MedPage Today column that two different researcher teams have stumbled upon what one of them describe as a "serendipitous" discovery of a hormone in their studies that actually works as the very mechanism behind why fat-burning is so functional on a low-carb diet.
The lead researcher on the first team, led by Dr. Eleftheria Maratos-Flier who serves as an investigator in the department of endocrinology, diabetes and metabolism at Beth Israel Deaconess Medical Center as well as an associate professor of medicine at Harvard Medical School, saw something peculiar happen to mice over a 30-day period that she fed a high-fat, low-carb diet--their lipid profile remained constant and didn't go up!
This coincides with a study conducted by Dr. Jeff Volek and Dr. Stephen Phinney that found people who ate a diet higher in saturated fat did not have an elevated presence of saturated fat in their blood--as has been previously theorized. This is why fat consumed does not make you fat.
Dr. Maratos-Flier says this seemingly contradictory finding has to do with a hormone called FGF21, or fibroblast growth factor 21. It is found in the liver and is responsible for producing ketones when people consume a low-carb diet. These ketone bodies are then used to provide as much as 70 percent of the energy needs of someone eating this way.
This discovery did not go unnoticed by the researchers. Unfortunately, instead of promoting the Atkins diet as a means for lowering body fat, they instead turned to the possibilities this discovery could have on future pharmaceutical opportunities.
"We think these findings would increase the desirability of a drug that (might work through this mechanism) to increase fat oxidation in the liver," Dr. Maratos-Flier said.
WHAT IN THE WORLD?!?! Why try to make a pill that will replicate what the Atkins diet has already been shown to do a beautiful job of doing, Dr. Maratos-Flier? This is just more irresponsible extrapolations pulled from an excellent study showing a high-fat, low-carb diet is beneficial. Get your head out of the sand already!
She does acknowledge that this switch to fat-burning mode in the mice only happened when FGF21 was found in higher concentration--on either a low-carb diet or during starvation. Contrary to what the naysayers say, these two are NOT the same.
The lead researcher on the second team, Dr. Steven Kliewer who is a professor of molecular biology at the Dallas, TX-based University of Texas Southwestern Medical Center, also found FGF21 breaks down stored fat in animals consuming a high-fat, low-carb diet as well as fasting.
"[A high-fat, low-carb diet] turned on a starvation response, even when the animals were feeding," Dr. Kliewer noticed. "They switched from using carbohydrates to fat stores as an energy supply."
Dr. Kliewer said this is a natural reaction in animals to a shortage of food which causes them to move less and sleep more in order to store up energy.
He was surprised that a single hormone could literally "flip the whole metabolic profile" and that it can actually serve as a balancing mechanism for consuming too many calories.
"What's really exciting is that mice with excess FGF21--even when they are fed--look like they are fasted," Dr. Kliewer found.
Somewhere up in heaven today, Dr. Atkins has got to be smiling from ear to ear. This exactly what he was talking about when he described his diet as giving people a "metabolic advantage." The fact that science is just now catching up to what the late great Dr. Robert C. Atkins was sharing decades ago proves he was a man long before his time.
Dr. Kliewer admitted that this fat-burning process "makes sense" when you stop and think about it.
"During fasting, the liver hormone communicates with adipose tissue to send fat to the liver," he said. "It turns on the metabolism of fat into ketone bodies--and at the same time, it sensitizes the animals to going into torpor to conserve energy."
He added that there is an "obvious possibility that FGF21 accounts for the proposed positive effect of the Atkins diet—including weight loss and an increase in [HDL] ‘good’ cholesterol."
While Dr. Kliewer states that FGF21 might explain why the Atkins diet works, Dr. Maratos-Flier brought up the ridiculous argument that this is only true in mice right now and it is unclear of the impact on humans.
Good grief, lady! Can't you even put out the notion that it is even POSSIBLE the same results could be true in humans as well? Sheeez! To her credit, Dr. Maratos-Flier is planning on study FGF21 levels in human subjects next over just a few days. How about long-term studies of weeks, months, and years, too, Dr. Maratos-Flier?
Both of these studies were funded by the National Institutes of Health (NIH) as well as Takeda Pharmaceuticals, the Robert A. Welch Foundation, the Betty Van Andel Foundation, the Smith Family Foundation Pinnacle Program Project Award from the American Diabetes Association, and the Howard Hughes Medical Institute.
The results of these studies were published in the June 2007 issue of the scientific journal Cell Metabolism. Check out the abstract for both studies by Dr. Maratos-Flier and Dr. Kliewer.
Describing this research as "the most exciting" study he has ever worked on, Dr. Kliewer wants to continue looking at the role of FGF21 in increasing lifespan.
"Starvation and restricted diet are linked to some fascinating physiology including longevity," he noted. "In the long term, I would like to investigate the role of FGF21 in aging, since caloric restriction has been linked to an extended life span in many species."
I don't know about the "caloric restriction" aspect of his research, but it certainly sounds fascinating to see a low-carb diet being observed in this manner. Who knows what the implications could be. We'll be watching, Dr. Kliewer!