Hunger and Satiety

Hunger and Satiety


Today I want you to meet Obese and Lean. These
two guys are pretty much identical, they have the same age and they have been exposed to
the exact same environmental conditions since they were born. Their genetic makeup is also
extremely similar, except for one thing. Obese lacks a receptor for leptin, a hormone secreted
by the adipose tissue which signals satiety. As a result of this little genetic defect,
Obese is always hungry, and while it has always been given the same amount of food as his
friend Lean, Lean would stop eating after a while, while Obese would keep going until
its food was over. If I offer a pellet of food to lean, he is only marginally interested.
But if I offer it to obese, well, look for yourself. As a result of this impaired satiety
reflex, and only because of that, already after two or three weeks of life, Obese became…
well, obese. Today, at 4 months of age, lean weighs in at 350 grams. While Obese, weighs
more than 670 grams. Hunger and satiety are crucial regulatory
mechanisms that greatly contribute to maintain a healthy body weight, or to disrupt it if
something goes wrong. The hunger and satiety center is located in
our brain, and specifically in the paraventricular nucleus of our hypothalamus, although other
regions of our brain are also involved in this regulatory activity. Our brain integrates
short and long term biological and psychosocial signals that influence our eating behavior
and metabolism. Hunger and appetite are our ‘go’ signal
for eating, while satiation and satiety are ‘stop’ signals.
Hunger is a strictly biological signal. It is defined as our biological drive to eat,
and is controlled by our internal hunger and satiety mechanisms. A group of chemicals in
our brain, called orexins, are released when our bloodstream, our digestive systems and
our energy stores send signals that it’s time to eat because we are beginning to run
out of energy and nutrients. The main orexin is the neuropeptide Y, NPY, a neurotransmitter
that relays the signal to eat more, causing hunger. Conversely, when our bloodstream,
our digestive system and our energy stores send signals that we still have plenty of
nutrients, anorexigenic chemicals are produced in our brain, such as alpha-melanotropin,
a hormone which does the exact opposite of the NPY, and relays the signal that we don’t
need to eat, causing satiety. What we eat, how much we eat, when we eat,
where we eat and why we eat, is what we call our eating behavior. As we will learn, eating
behavior is determined biologically, but also psychologically and socially.
If hunger is a strictly biological signal, appetite is the psychosocial drive to eat,
mainly controlled by external influences, which we will explore more in detail in the
next lesson. Of course appetite is also mediated by biological signals, such as the release
of endorphins, our brain’s pleasure molecules. Let’s now examine our ‘stop eating’
signals. Satiation is the perception of fullness that
develops during a meal and determines its duration. These short term, ‘end of meal’
signals are both psychological, mechanical and hormonal. The main psychological signal
is our perception of the amount of food we have been eating, and as we will learn, our
brain mainly takes into account the volume of food and the number of servings, and not
so much the caloric density or the nutrient content. The main mechanical signal is the
distention of the walls of our stomach and intestine, caused by the presence of food.
Two important hormonal signals are the release of cholecystokinin (CCK) and of PYY3-36 that
our intestine releases into our bloodstream at the passage of food. By inhibiting release
of neuropeptide Y in our brain, these signals reduce hunger. While satiation is a short-term feeling that
develops during the meal, satiety is the perception of fullness after the meal has ended and determines
the interval between two meals. Sensors in our brain and liver constantly monitor blood
glucose and insulin levels, and when these are low, our liver starts gluconeogenesis
to make some new glucose, and our brain induces hunger to get some more from food. Other sensors
in our digestive tract constantly monitor stomach and intestinal filling, and when these
are empty, our stomach releases the hormone ghrelin, which induces hunger by promoting
release of neuropeptide Y in our brain. The nutrient composition of the food we eat
influences our hunger and satiety signals. Some nutrients are more satiating in the short
term, while others have a more of a long term effect. For example, fiber strongly induces
satiation, but is very weak on satiety. If we only eat a veggie salad, it will fill us
up quickly, but we will be hungry again soon. In contrast, lipids have a weak effect on
satiation, but a strong effect on satiety. If we only eat a high fat food for lunch,
such as nuts, by the time we feel full we have already eaten much more calories than
we need. But at least, we will not be hungry again for quite a while. Carbohydrates are
not very satiating: they have a medium effect on satiation, and a weak effect on satiety.
Finally, proteins have the stronger satiating effect of all nutrients, because they strongly
induce both short-term satiation and longer-term satiety. We also have signals that operate in the longer
term to regulate hunger and satiety, and a very important one is leptin. Leptin is a
hormone secreted primarily by our adipose tissue, and it targets the brain to decrease
hunger. Our brain, however, is much more sensitive to variations in leptin concentrations, providing
for a very smart homeostatic mechanism. When we overeat over the long term and our adipose
tissue grows, our leptin concentrations increase which causes our hunger to decrease. Conversely,
when we start losing adipose tissue and therefore our leptin levels drop, our brain gets the
message that we’d better start eating a little bit more, and our hunger increases.
While this system works very well to protect us from under-eating, as many people on weight
loss diets can witness, it is unfortunately not so efficient the other way around. In
fact, obese people, who have a lot of adipose tissue, also have a lot of leptin around,
but this has no effect on their hunger because when it is overexposed to leptin, our brain
quickly becomes insensitive to it, a situation called leptin resistance. Besides not doing
anything useful, all this circulating leptin in obese individuals is actually harmful,
because leptin is a pro-inflammatory molecule. As you can easily understand, giving supplemental
leptin to obese people has no effect whatsoever on their hunger, except for a very small percentage
of obese individuals who became obese precisely because they lack leptin, like our friend
Obese. Another kind of stop eating signal is specific
satiety, which mostly determines the composition of our meal, rather than its duration. Specific
satiety is the perception of fullness that develops during consumption of one food item
in particular. As we keep eating one specific food, its palatability decreases until we
feel ‘full’ for that specific food, although we still have appetite for other foods. If
I start eating carrots, after a while I’ll be like, that’s enough, if I see one more
carrot it will make me sick. But if they offer me a slice of cheesecake, chances are I still
have an appetite for it. This is a very important physiological mechanism to induce variety
in our diet, and therefore maximize our chance of getting all the nutrients we need from
different foods. It is also used as a little trick by many popular weight loss diets that
do not restrict the amount, but the variety of food items we can eat: if we can eat unlimited
amounts, but only of cabbage soup, we soon get bored and end up eating less calories
anyways. Our biological regulation of eating behavior
is very effective in protecting us from under-eating, but is very weak against overconsumption.
Don’t forget that the human body is evolutionarily programmed to accumulate, and is much less
concerned with avoiding excess food. And as we learned today, biologically we only
regulate hunger, but eating behavior is also strongly driven by psychosocial factors that
determine appetite. We will explore some of these factors over the next few videos.

19 Replies to “Hunger and Satiety

  1. Apprezzo tantissimo il suo lavoro e questo nuovo canale, ma avrei fatto a meno delle cavie. Ma anche ammettendo le cavie, è proprio necessario tenerle in gabbie così piccole e prive di stimoli o occasioni di socializzazione? Bah. 

  2. Thank you so much for this helpful, easy and informating courses!!! This is the only really scientific and correct information I could find throught the whole internet! Thanks ! 🙂

  3. so if fat satiating for longer period of times is it ok to eat high calorie densed food,and it will keep hunger away for a long time? thanks

  4. Does anyone know if an extensive list has been made ? I'm talking like 200-300 foods, or at least 100.

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