Winning the Battle of the Bulge: We're a Scrimmage Closer to Victory | Saint Louis University
April 27, 2004
Winning the Battle of the Bulge: We're a Scrimmage Closer to Victory
"We feel that we now understand what part of the system is broken -- why leptin isn't working." -- William A. Banks, M.D.
ST. LOUIS -- Saint Louis University researchers believe they've won a major skirmish in the battle of the bulge, and their findings are published in the May issue of Diabetes.
"We figured out how obesity occurs," says William A. Banks, M.D., professor of geriatrics in the department of internal medicine and professor of pharmacological and physiological science at Saint Louis University School of Medicine. "The next step is coming up with the solution."
The scientists used mice to look at how leptin, a hormone secreted by fat cells that tells us to stop eating, gets into the brain. They found that in obese mice, high triglycerides, a type of fat in the bloodstream, prevents leptin from getting into the brain, where it can do its work in turning off feeding and burning calories.
"High triglycerides are blocking the leptin from getting into the brain. If leptin can't get into the brain, it can't tell you to stop eating," says Banks, who is principal investigator and a staff physician at Veterans Affairs Medical Center in St. Louis.
"This is a big deal. We now know what is keeping leptin from getting to where it needs to do its work."
Paradoxically high triglycerides occur in both fat and starving animals and make the brain think the body's starving so the animal keeps eating, which makes it gain more weight.
I read this article and thought, wow, new discovery? But it sounded like something I read before. Viola, here's a Dr. Eades article from 5 years ago where he says the same thing. Some discovery. Oh, and of course the answer isn't to lower triglycerides through low carb diets, but to invent a new pill.
Leptin, low-carb and hunger
So as leptin levels wax and wane, so does your sense of hunger and even, to an extent, your metabolic rate.
Where does the low-carb diet fit into the picture?
There is a critical point in the cycle described above. That critical point is when the leptin crosses the BBB. If the leptin can’t get across the BBB, it can’t get to the brain. If it doesn’t get to the brain, it doesn’t shut off the hunger response irrespective of how much is circulating in the blood.
Most obese people find themselves in this very situation: high blood levels of leptin but still hungry. And eating makes more fat, which makes more leptin, which should shut off the hunger response, but it doesn’t because the ever increasing levels of leptin telling the brain to tell the obese person to quit eating don’t get to the brain to do their job.
Research done a couple of years ago in St. Louis and in Japan pinpointed the problem. Triglycerides – fat circulating in the blood – interrupts the passage of leptin across the BBB. If trigylcerides are high, which they are in most obese people, then, basically, they block the movement of leptin into the brain. So, leptin levels are elevated in the blood, and triglycerides keep the leptin from getting to where it needs to get to shut off hunger. (click here for the abstract and full text of this research paper.)
We all know that the commonest lab finding in people following a low-carb diet is a dramatic reduction in triglyceride levels. This reduction in triglycerides allows the leptin that is already circulating in relatively large amounts to get through to the brain where it can reduce hunger. I believe that this reduction in triglycerides (which happens fairly quickly) is the primary reason that people substantially decrease their hunger on low-carb diets. And remember from the graphic above that leptin – once it gets to the brain – actually increases thermogenesis as well, which means that the metabolic rate increases.