PTCers interested in physiological control mechanisms should find the following research article quite interesting:
B. Silvano Zanutto and John E. R. Staddon (2007). Bang-bang control of feeding: Role of hypothalamic and satiety signals. PLoS Comput Biol 3(6): e127. doi: 10.1371/journal.pcbi.0030127
It’s a free download at http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.0030097 . What Zanutto and Staddon have done is create a control model of feeding that involves a cascade of up to three leaky integrators representing various compartments through which food is processed once consumed. The model is used to account for meal-consumption patterns of rats and includes a manipulation in which the animals are allowed to feed freely but occasionally, access to food is briefly disturbed just after initiation of a bout of feeding. Here is the author summary:
Rats, people, and many other omnivores eat in meals rather than continuously. We show by experimental test that eating in meals is regulated by a simple bang-bang control system, an idea foreshadowed by Le Magnen and many others, shown by us to account for a wide range of behavioral data, but never explicitly tested or tied to neurophysiological facts. The hypothesis is simply that the tendency to eat rises with time at a rate determined by satiety signals. When these signals fall below a set point, eating begins, in on–off fashion. The delayed sequelae of eating increment the satiety signals, which eventually turn eating off. Thus, under free conditions, the organism eats in bouts separated by noneating activities. We report an experiment with rats to test novel predictions about meal patterns that are not explained by existing homeostatic approaches. Access to food was systematically but unpredictably interrupted just as the animal tried to start a new meal. A simple bang-bang model fits the resulting meal-pattern data well, and its elements can be identified with neurophysiological processes. Hypothalamic inputs can provide the set point for longer-term regulation carried out by a comparator in the hindbrain. Delayed gustatory and gastrointestinal aftereffects of eating act via the nucleus of the solitary tract and other hindbrain regions as neural feedback governing short-term regulation. In this way, the model forges real links between a functioning feedback mechanism, neuro–hormonal data, and both short-term (meals) and long-term (eating-rate regulation) behavioral data.
BA: PTCers interested in physiological control mechanisms should find the following research article quite interesting:
B. Silvano Zanutto and John E. R. Staddon (2007). Bang-bang control of feeding: Role of hypothalamic and satiety signals. PLoS Comput Biol 3(6): e127. doi: 10.1371/journal.pcbi.0030127
RM: Interesting indeed. I’ll have to read the paper in more detail to see what data their model accounts for. But the model itself looks like it could use some improvement. Here’s their diagram of the model:
RM: This is a model of a system that controls the “satiety signal” keeping it at the reference (set point). So “satiety” is the controlled perception but the model says nothing about what it is a perception of. Since this is the short term regulation control loop I assume satiety is a perception of something like stomach distention rather than glucose level.
RM: Stomach distension makes sense as the basis of the satiety perception because satiety depends, after a delay,on “eating”. The more you eat, integrated over time, the greater the distention and, thus, the greater the satiety Presumably the delay box includes the disturbances to the controlled variable, which would be externally imposed delays in eating as well as digestive reduction of stomach distension.
RM: The set point for satiety is apparently set by a higher level system – the long term system that is presumably controlling blood sugar level. So this is a two level model that shows only one level.
RM: Since the model doesn’t show the output variable or environmental correlate of the controlled variable (satiety), I have no idea how they tested it. But I think they could be helped out a lot if you could show them that eating is the control of input, not output. Their language in the “author summary” shows that they think of this model as controlling eating, not satiety. Here’s the sentence that betrays their conceptual orientation:
Rats, people, and many other omnivores eat in meals rather than continuously. We show by experimental test that eating in meals is regulated by a simple bang-bang control system
RM: No, it’s not eating in meals that is regulated by the control system; it’s the perceptual consequences of consuming food (blood sugar level, stomach distension, etc – to be determined by the test for controlled variables ) that are regulated (controlled) by eating in meals.
Best
Rick
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Richard S. Marken, Ph.D.
Author of Doing Research on Purpose.
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