A recent study props up the underlying principle of low-carb, high-protein dieting – possibly giving vanishing low-carb fad diets, such as the once-fashionable Atkins diet, one last laugh.
Low-carb diets lost much of their popularity as critics said their approach puts followers at higher risk of clogged arteries and heart attack in the long-term. Atkins Nutritionals, for one, filed for bankruptcy last year only to re-emerge in January with a new mission to promote 'tasty, portable nutrition'.
The recent findings by scientists at the University College London (UCL) could vindicate, at least partially, these recent dieting fads as they have illustrated more clearly how high-protein diets can be effective in combating obesity.
How the study was done
The study, published in the September issue of Cell Metabolism, set out to investigate how increased dietary protein increases satiety, hypothesising that gut hormones could mediate the differential satiation produced by protein, fat, and carbohydrates.
The Medical Research Council team of researchers, led by Dr Rachel Batterham, linked high-protein diets to higher levels of the gut hormone known as PYY. Their work suggests PYY is an important appetite suppressor that sends signals to the brain leading to a feeling of fullness.
"In summary, our current studies have established the physiological role of PYY as a regulator of energy homeostasis and demonstrated that it mediates the satiating and weight-reducing effects of dietary protein," wrote the study authors.
Ten healthy normal-weight and ten obese male volunteers were given an isocaloric meal, high in one macronutrient - protein, fat or carbohydrate - and researchers then analysed their blood samples.
High-protein: reduction in hunger
The high-protein diet resulted in the greatest reduction in hunger in both normal and obese participants. The high-protein meal resulted in the largest increase in both total plasma PYY and integrated PYY levels in both groups, although post-meal levels were lower in obese subjects.
"These findings suggested that PYY could mediate the satiating effects of protein in humans," explained the authors. "We therefore developed a rodent experimental model in which to investigate this possibility."
As such, genetically modified mice that lacked the PYY hormone were then created. The PYY deficient mice ate more than regular mice and, as a result, became obese.
The mice were fed high-fat normal-protein, high-fat high-protein, low-fat normal-protein or low-fat high-protein diets.
Mice developed marked obesity
The researchers found the PYY null mice were hyperphagic and developed marked obesity but were hypersensitive to exogenous PYY.
They then administered PYY to these mice. The mice's food intake subsequently decreased to normal levels as did their weight. When they no longer received PYY, the amount they ate went up again at the same time as their weight.
"Chronic treatment with PYY reverses their obesity phenotype," the authors commented on the obese mice. "These findings provide compelling evidence that PYY is a physiologically relevant regulator of food intake and body weight."
Clues to the obesity epidemic
The findings could help explain the current obesity epidemic plaguing South Africa, Europe and North America. Statistics show diets have shifted from being protein-rich to carbohydrate-rich, according to the study, and carbohydrates do not curb appetite in the same way protein does, resulting in people eating more to compensate.
Currently, the average Western diet derives 49 percent of energy from carbohydrates, 35 percent from fat, and 16 percent from protein, cites the study.
"This research suggests that an increase in the protein content of the diet may help tackle obesity," said Batterham. "However, large scale clinical trials are needed before high-protein, low-fat diets can be recommended." - (Decision News Media, September 2006)
Rachel L. Batterham et al. "Critical role for peptide YY in protein-mediated satiation and body-weight regulation." Cell Metabolism. Vol 4: 223-233, September 2006.