|There are millions of ways to con- sume 100kcal and volume isn't the only difference (img greatist.com)|
I guess, it's not debatable that replacing trashy foods with healthy ones is the most important factor. We have all heard about the beneficial effects "high volume foods" and the downsides of the average high energy + low nutrient 100kcal junk-food snack. But how important is the volume, actually? Isn't food "quality" (whatever that may be) all that counts?
It's surprisingly difficult to answer this question and after reviewing the most important studies, I have to say that I still can't tell for sure how important the volume is.
|Figure 1: Effects of pylorectomy (removal of the part of the stomach that contains the vagal nerves) and vagal deafferetation on the ability of CCK to affect liquid food intake in rats (Moran. 1988)|
What we do know is that electrophysiological recording studies as well as behavioral studies have found that the effect of a given dose of cholecystokinin (CCK) is increased in the presence of stomach stretch (Schwartz. 1993 & 1995) and disrupted, when the vagus nerve is damaged or the NTS lesioned (Edwards. 1986; Moran. 1988; Smith. 1985).
With CCK being a major satiety hormone (and on top one that actually does what it's name implies, i.e. signal satiety) it appears to be quite certain that the multiplying effect the mechanical stretch exerts on the satiety effect of CCK is one of the secondary mechanisms by which eating high volume foods keep you lean.
Do you remember? You've read about a couple of things that will increase the release of CCK and would thus synergize with the effects of what I would like to call "high volume eating": (1) The pre-ingestion of protein before a meal | learn more, (2) Arginine, lysine and glutamic acid | learn more, and lastly and unsurprisingly a gastric bypass operation | learn more. Another well-known trigger of CCK release is the ingestion of fatty acids (low amounts suffice; long chain polyunsaturated fatty acids are particularly effective; Gribble. 2012) - is not satiating.In view of the fact that the NTR, ie. the nucleus tractus solitarius, integrates (adds up and processes) a whole host of signals from the gastro-intestinal tract, it's also hardly surprising that a gastric bypass surgery and the corresponding increase in stretch per volume unit of food that has just recently been shown to change not just the satiety response to food but also the way foods taste and smell for patients who have undergone Roux-en-Y gastric bypass surgery (learn more in the SuppVersity Facebook News).
learn more about GLP-1) are the reduction of gastric emptying (Read. 1994), and other interactions between the vagus nerve and the brain, which include aside from directly satiety related mechanisms also the activation of serotonergic neurons (remember: serotonin is the happy hormone) in the brain (Mazda. 2004).
- Berthoud, Hans-Rudolf, Penny A. Lynn, and L. Ashley Blackshaw. "Vagal and spinal mechanosensors in the rat stomach and colon have multiple receptive fields." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280.5 (2001): R1371-R1381.
- Edwards, et al. "Dorsomedial hindbrain participation in cholecystokinin-induced satiety." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251.5 (1986): R971-R977.
- Gribble, Fiona M. "The gut endocrine system as a coordinator of postprandial nutrient homoeostasis." Proceedings of the Nutrition Society 71.4 (2012): 456.
- Kim, Doe‐Young, et al. "Is there a role for gastric accommodation and satiety in asymptomatic obese people?." Obesity research 9.11 (2001): 655-661.
- Mazda, Takayuki, et al. "Gastric distension-induced release of 5-HT stimulates c-fos expression in specific brain nuclei via 5-HT3 receptors in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 287.1 (2004): G228-G235.
- Moran, Timothy H., et al. "Pylorectomy reduces the satiety action of cholecystokinin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255.6 (1988): R1059-R1063.
- Näslund, Erik, and Per M. Hellström. "Appetite signaling: from gut peptides and enteric nerves to brain." Physiology & behavior 92.1 (2007): 256-262.
- Phillips, Robert J., and Terry L. Powley. "Tension and stretch receptors in gastrointestinal smooth muscle: re-evaluating vagal mechanoreceptor electrophysiology." Brain research reviews 34.1 (2000): 1-26.
- Read, Nicholas, Stephen French, and Karen Cunningham. "The role of the gut in regulating food intake in man." Nutrition reviews 52.1 (1994): 1-10.
- Schwartz, Gary J., et al. "Gastric loads and cholecystokinin synergistically stimulate rat gastric vagal afferents." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265.4 (1993): R872-R876.
- Schwartz, Gary J., Gervais Tougas, and Timothy H. Moran. "Integration of vagal afferent responses to duodenal loads and exogenous CCK in rats." Peptides 16.4 (1995): 707-711.
- Smith, Gerard P, et al. "Afferent axons in abdominal vagus mediate satiety effect of cholecystokinin in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249.5 (1985): R638-R641.
- Woods, Stephen C. "Gastrointestinal satiety signals I. An overview of gastrointestinal signals that influence food intake." American Journal of Physiology-Gastrointestinal and Liver Physiology 286.1 (2004): G7-G13.