A new way of looking at eating

Abstract
The analysis of meals, especially of spontaneous meals, has long had a problematic place in the behavioral neuroscience of eating. Only a small minority of eating researchers now, or ever, have concerned themselves with meal patterns. On first glance this seems paradoxical. After all, eating occurs only, or mainly, as meals, so why are meals not the major focus of eating research? Many factors contribute to this situation. I name five: First, identifying the basic unconditioned physiological stimuli controlling meals has been agonizingly slow and difficult. By the 1970s the classic gastric and glucostatic accounts of meal initiation and termination ([7][1], [21][2]) were no longer influential, and only in the last 10 years have a few alternative mechanisms been well established (e.g., 6, 15, 28). The poor understanding of the physiological basis for meals rendered meal pattern analysis uninteresting for many investigators. Second, in contrast to the poorly elaborated physiological mechanisms, environmental, ecological or “economic” variables, such as caging conditions, foraging cost, etc., very potently affected meal patterns ([10][3], [22][4]). Third, even under the simplest conditions, meal pattern analysis did not produce consistent functional relationships. Perhaps the outstanding example concerns early reports ([19][5], [20][6]) that the durations of intermeal intervals were closely correlated with the size of the preceding meal (the “satiety ratio”), suggesting that meal initiation is triggered by some nutritional consequence of depletion of immediately preceding intake. This finding proved discouragingly difficult to replicate ([8][7], [14][8], [23][9]). Fourth, there was little unanimity as to the appropriate definition for meals. Furthermore, most definitions were arbitrary, and few were biologically based [an important exception is the criterion that a meal ends when the sequence of postprandial satiety behaviors appears ([3][10]), but biological definition has not been used in spontaneous eating]. Finally, there were no points of contact between the various definitions. Fifth, although formal theories of meal size appeared and were tested (e.g., 12, 27), there was no similar progress for rats’ meal patterns. Perhaps for this reason, formally questionable mathematical procedures were tolerated. For example, the most popular quantitative method applied to meal pattern definition is the log survivorship analysis ([9][11], [26][12]), which is suspect because exponential functions used to fit such data produce the theoretically disturbing prediction that the probability of initiating a new meal stays constant as time since the last meal passes, rather than increasing with time as predicted by most, if not all, concepts of hunger and satiety. Thus meal pattern analysis was an ugly duckling. For more than 50 years there has been a more attractive alternative: total food intake. Hypothalamic lesions that made animals eat to obesity or starve to emaciation were discovered more than 50 years ago ([2][13], [5][14], [18][15]). At the same time, convincing arguments were presented that animals eat for calories ([1][16]) and that body adiposity is a biologically regulated variable, like blood oxygen content ([17][17]). Thus, both a problem and a theoretical approach appeared for eating that was couched in terms of total food intake (daily?, weekly? monthly?) expressed in units of metabolizable energy content, without reference to meals. Nor was theoretical support for behavior-less analysis of eating lacking. Stellar’s ([29][18]) theory of hypothalamic centers for motivation focused on overall drive and explicitly omitted the effector mechanisms involved. More generally, overenthusiastic application of cybernetics and control theory ([30][19], [33][20]) often transmogrified biology into information processing. The influence of the kinds of ideas that support analysis of total food intake rather than meals seemed to be waning in the 1980s but has enjoyed a major renaissance since modern molecular biology has revolutionized the science of eating. Given all of this, why bother with meals? The reason is in fact rather obvious. The meal is a biological unit of eating behavior and therefore should not be ignored. “Why?” was succinctly stated in 1955 by John Brobeck ([4][21]) in the first lines of his address at a major conference on the regulation of eating: “Nearly all of the published studies of the regulation of food intake neglect the fact that the total amount of food eating is always the product of two factors, the number of meals multiplied by the intake of the average meal. … Any procedure altering food intake does so through some change in one of both of these.” That Brobeck first reported that ventromedial hypothalamic lesions increase body weight by increasing total food intake ([5][14]) and that lateral hypothalamic lesions decrease total food intake and body weight ([2][13]), and, as far as I know, himself never measured meal patterns is perhaps ironic, but establishes his credentials as an impartial expert. Brobeck made this point because he was interested in the brain and recognized that a neurological analysis of eating needs to be performed at the level of what the brain produces, that is, movements. A neuroscience of eating that does not include behavior will sooner or later come to a dead end before reaching its goal. It may be argued that bites, chews, licks, and swallows are the movements of eating, not meals. These microstructural elements of eating are integral parts of the problem and provide a direct link from behavior through lower motor neurons into the interneuronal networks controlling them ([13][22], [16][23], [27][24]). However, they alone will fail to account for the molar rhythms of eating, which indicates that a supervening component of the controlling interneuronal networks, that may perhaps...

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