Have you noticed that you are ravenously hungry an hour or two after certain meals? Or that you stay fuller, longer after others? Many people have learned that adding protein to their breakfast meal is the best insurance against the mid-morning munchies. And a bit of chicken in your lunchtime salad may help you make it to dinner without a trip to the vending machines.
Protein, it turns out, enhances satiety (the feeling of fullness) and helps you lose weight. Scientists from University College London think they know why. In a paper published in the September 2006 online journal, Cell Metabolism, Rachel Batterham and colleagues review the role of a gut hormone (peptide YY or PYY, for short) in mediating the sensation of satiety caused by ingestion of protein meals.
Hormonal control of appetite
PYY is a hormone that is released from the gut after eating a meal. It apparently acts on the brain to cause satiety. The amount of PYY released is dependent on the composition of the meal. High protein meals are associated with the greatest release of PYY compared to the amount of PYY released after high fat or high carbohydrate meals.
In experimental subjects, high protein meals also cause the greatest reduction in hunger, measured by a hunger score, in both normal weight and obese people. Plasma PYY levels, however, are lower in obese people compared to normal weight people.
Control of appetite is quite complex. Humans evolved in an environment where food was in short supply and required a lot of effort to obtain. Thus, the need to have interacting mechanisms to ensure we will go out and chase down the next meal in order to survive another day. Unfortunately, in this day of easy-to-obtain, energy dense food, these control mechanisms can make it hard to maintain a healthy weight.
Other gut hormones that are involved in appetite control include:
- Ghrelin, a stomach hormone that increases hunger and food intake. Ghrelin is widely thought to be the hormonal mediator of weight regain after weight loss.
- Cholecystokinin (CCK) comes from the duodenum, the part of the intestinal tract that links to the stomach. CCK causes short-term satiety.
- Glucagon-like peptide 1 (GLP-1) and oxyntomodulin (don’t you just love these names?) also come from the gut. Both are associated with decreased food intake.
Leaning more from mice
In order to more fully understand the role of PYY in protein-mediated satiety, the researchers conducted several studies in mice. First, they determined that adding dietary protein to mouse meals was associated with an increase in PYY levels, decreased food intake, and reduced adiposity (fatness).
Next, the researchers developed a strain of mice that were unable to make PYY. They called these mice “PYY null mice”. These mice were resistant to both the satiating and weight-reducing effects of protein meals. They became very fat. When PYY was injected into the null mice, they lost the weight. This series of experiments suggests that PPY is the mediator of protein-induced satiety and weight loss.
What does this mean for humans?
Mice aren’t human and PYY null mice are not “normal” mice. Further, most people eat meals that vary in the mix of protein, carbohydrate, and fat. So it may turn out that these results cannot be simply translated into a definitive weight loss recommendation. We do know that people lose weight quicker on a high protein diet, such as the Atkins diet, but this diet is no more effective than reduced calorie diets in the long run. It is also very difficult for people to stick with an Atkins-type diet for prolonged periods of time.
I think it is safe to say that if you find, by trial and error, that adding a little extra protein to your meals helps to keep you fuller longer, then, by all means, include it in your otherwise balanced diet. But be sure you watch your portion sizes and keep on counting those calories.