Tuesday, April 22, 2014

True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean. Bonus-Q: Will a High Volume Make Your Stomach Go Baggy & Mess Up Your Satiety Response?

There are millions of ways to con- sume 100kcal and volume isn't the only difference (img greatist.com)
I have repeatedly pointed out that filling yourself up on vegetables and other high volume, high nutrient (vitamins, minerals, polyphenols, etc.), low energy foods is one of the fundamental principles of weight management. The question that remains, though, is whether this principle is so effective because of the food we eat (tons of veggies), or rather due to the fact that there is no room for the foods we thusly don't eat (the typical processed junk)?

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?
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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 I can tell you, though, is that it appears to be certain that the mechanical stretch will be detected by vagal affarent endings in the stomach (Phillips. 2000; Berthoud. 2001). These "stretch detectors" are hard-wired to your brain, where they are processed in the so-called "nucleus tractus solitarius" (Näslund. 2007). Unfortunately, the exact role of the "nucleus tractus solitarius" in the satiety response is not even partly understood.

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).
Figure 2: Model depicting signals that influence food intake. Not all elements are relevant in the context of this article - focus on the way the satiety signals that are generated in the gastrointestinal (GI) tract during meals provide information about mechanical (e.g., stomach stretch, volume) and chemical properties of the food to the brain (Woods. 2004)
Other mechanisms by which the gastric stretch may contribute to an increase in satiety / reduction in food intake and, via the release of GLP-1 and other glucose regulating satiety hormones (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).
Bonus question: Is high volume eating setting you up for obesity? You could argue that the constant gastric distension and consequently increased postprandial gastric accommodation will reduce the satiety response to small calorie dense meals. Now aside from the fact that you will get fat, no matter what if you eat those on a daily basis, a study from the Gastroenterology Research Unit in Rochester and the Mayo Clinic did not find a sign of increased postprandial gastric accommodation or reduced satiety in any of of their 13 obese subjects (Kim. 2012).
So, yes! There is more to eating tons of veggies than not eating tons of other food. Moreover, although we don't yet know exactly what this "more" is, we can already say that all the existing evidence appears to support that it the high food volume, the stretch of the stomach and the vagally mediated downstream effects on the release and effect of our satiety hormones (incretins) is one of the factors that contribute to the ability of high volume, high nutrient, low energy foods to keep you lean.

On it's own, the multi-layered stretch-response is probably significantly less important than the reduction in junk-food intake. In conjunction with the synergistic effects of a high protein diet, and a reasonable amount of long-chain fatty acids in the diet, it could yet be what distinguishes people who have to resort to a gastric bypass as a last resort to save their lives from those individuals, who manage to flip the switch, turn their life around and lose their life-threatening overweight without the help of a surgeon.
References:
  • 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.