Our regulation of eating depends upon a complex accord of signaling chemicals - hormones.

The main trigger of appetite is ghrelin, which has acylated form and unacylated, the latter acts as an abolisher to the first. But there are about two dozen chemicals that play a supporting role, and about the same number of appetite suppressants like insulin (produced in the pancreas), leptin (in fat cells), and PYY and oxyntomodulin (in the digestive system). Such hormones suppress ghrelin release. If anything is wrong in this regulative system, overeating can be expected.

All these hormones travel through the liquids of the body with these messages and provide communication between the brain and the digestive system and its microbiome. If the main messengers are in low concentrations, others take their role.

Compared to other micronutrients, fats are less effective in suppressing hunger. Sugar and protein cause fast 70-percent drop in ghrelin both in rodents and humans, and fat reduces it much slower and only by half. Background ghrelin concentrations, pre-breakfast, rise as most people lose weight. But after several months of a weight-reducing low-fat diet, the levels remained unchanged. Simple sugars, particularly in isolated form, can affect choices of food and its amount, even for the next day. After a drink high in fructose, people may choose fattier foods than after one glucose-sweetened.

Heavy people misread or ignore hunger and satiety signals. Obese individuals usually have the lowest ghrelin levels, and anorexics very high. By normal-weight, more ghrelin production is suppressed while consuming more  calories. When overweight, ghrelin drops the same after all meals - the same as in regular-weight people after a 1,000-calory meal.

Food preferences, feeding-regulating hormones, and gut-brain signaling depend on sleep too.

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