Milk Proteins and Appetite Control
In addition to the direct effects of dairy protein on metabolic health, milk proteins may indirectly drive improvements in metabolic control through the enhancement of the control of appetite and/or other mechanisms which aid changes in both body weight and composition. High-protein foods have long been shown to have favourable effects on satiety, and whilst not all studies show suppression of food intake, altering the diet in favour of a higher protein component may well have a role to play in weight control. The significant advantage of a high dairy diet for appetite suppression and weight loss is the anabolic effect of dairy BCAAs on lean body mass. BCAAs enhance muscle protein synthesis and skeletal muscle mass, and may protect against loss of lean mass during periods of weight loss. As the largest organ group in the body and a highly metabolically active tissue, protection of skeletal mass may in turn contribute to an improvement in whole body metabolic health.
Whether different protein types have different effects on food intake however is not as yet well demonstrated, although there are some studies which have shown greater satiety for some dairy proteins relative to soy protein or other non-dairy proteins. Interestingly skimmed milk containing both whey protein and casein has been shown to decrease intake more than either protein alone in a study of isoenergetic preloads, whilst in another study whey protein in turn has been shown to suppress intake more than casein. Various whey protein-derived fractions may also have differential effects on satiety, including GMP which has long been purported to suppress food intake. Supportive evidence however is lacking. In an isoenergetic study of whey protein, whey protein plus GMP, whey protein-derived alpha-lactalbumin (α-lac), casein and non-dairy soy protein, it was α-lac that was shown to suppress intake relative to the other fractions, whilst in a study comparing various forms of GMP no differential effects on intake were reported. In a recent study of overweight women from our laboratory we also found no differential effect of GMP on energy intake when we gave matched beverages containing 25 g of whey protein concentrate, GMP, beta-lactoglobulin (β-lac) and colostrum-derived whey protein, although greater fullness was induced by β-lac.
In one of the early studies, protein-induced appetite suppression was attributed to both an altered rate of gastric emptying and an increase in postprandial serum AA concentrations following whey protein consumption. Differential effects have also been attributed to threshold concentrations of total serum AAs in more recent studies of whey protein-induced hunger suppression when whey and casein were given in a mixed preload meal. Interestingly in this study a lower dose (15 g, 10 en% protein) had a greater effect than a higher dose (38 g, 25 en% protein). Despite some differential effects of whey protein fractions in our recent study, we were unable to find a relationship between circulating levels of total AAs and measures of either hunger, satiety or food intake. It is possible that tryptophan may be the most important of the AAs for appetite suppression since 5-hydroxytryptophan (5HT, serotonin) is an established appetite-modulating neurotransmitter, but this remains as yet unsubstantiated. Other postulated mechanisms include regulation of satiety by the gastrointestinal (GI) peptides such as glucagon like peptide-1 (GLP-1), CCK and peptide YY (PYY). Circulating levels of these peptides clearly are altered following a meal where they have a role in digestion, absorption and the metabolic fate of ingested nutrients, but there remains questions around their role in the control of hunger, satiety and eating behavior. Our review of the literature and that of others leads to the conclusion that the role played by these peptides in the control of food intake is poorly demonstrated. De Graaf et al., observed that peptide concentrations induced through exogenous (pharmaceutical) administration are several-fold greater than those which occur when a meal is consumed, Whilst GLP-1 and PYY have clear anorectic effects at high pharmacological levels, following a meal blood concentrations remain relatively low and neither is likely to contribute significantly to the satiating effect of protein or other macronutrients. Circulating CCK levels following a high protein meal are closer to those achieved following exogenous infusion, yet the evidence that CCK is a critical driver in human satiety also remains elusive.
Unsurprisingly, the postprandial effects of dairy protein on GI hormones and energy intake are mixed, with changes in peptide concentrations rarely driving predictable changes in energy intake. For example, in a study of lean and obese men, 50 g of whey protein resulted in a prolonged postprandial suppression of ghrelin, increased GLP-1 and CCK, and as hypothesized, decreased energy intake of ~10%. Conversely, a study in obese men reported that 50 g whey protein resulted in a prolonged suppression of ghrelin, elevation of GLP-1 and CCK, but no detectable changes in energy intake. Hence, changes in gut satiety peptides in response to pre-meal protein beverages or after a meal do not reliably translate into changes in subjective appetite and satiety ratings or energy intake.