hunger, eating and health Flashcards
energy is delivered to the body in three forms:
(1) lipids (fats), (2) amino acids (the breakdown products of proteins), and (3) glucose (a simple sugar that is the breakdown product of complex carbohydrates, that is, starches and sugars).
gut microbiome
the bacteria and other organisms that live in our gastrointestinal tract. Much of the work of breaking down the food we ingest is done by the constituents of our gut microbiome.
Energy is stored in three forms:
fats, glycogen, and proteins. Most of the body’s energy reserves are stored as fats, relatively little as glycogen and proteins (see Figure 12.2). Thus, changes in the body weights of adult humans are largely a consequence of changes in the amount of their stored body fat.
two reasons why fat, rather than glycogen, is the primary mode of energy storage:
(1) A gram of fat can store almost twice as much energy as a gram of glycogen, and (2) glycogen, unlike fat, attracts and holds substantial quantities of water. Consequently, if all your fat calories were stored as glycogen, you would likely weigh well over 275 kilograms (600 pounds).
but glycogen is very readily concerted to glucose (body’s main directly utilizable source of energy)
hree phases of energy metabolism.
- The cephalic phase is the preparatory phase; it often begins with the sight, smell, or even just the thought of food, and it ends when the food starts to be absorbed into the bloodstream.
- The absorptive phase is the period during which the energy absorbed into the bloodstream from the meal is meeting the body’s immediate energy needs.
- The fasting phase is the period during which all of the unstored energy from the previous meal has been used and the body is withdrawing energy from its reserves to meet its immediate energy requirements; it ends with the beginning of the next cephalic phase.
During periods of rapid weight gain, people often go directly from one absorptive phase into the next cephalic phase, without experiencing an intervening fasting phase.
The flow of energy during the three phases of energy metabolism is controlled by two pancreatic hormones: insulin and glucagon. During the cephalic and absorptive phases, the pancreas releases a great deal of insulin into the bloodstream and very little glucagon. Insulin does three things: (1) It promotes the use of glucose as the primary source of energy by the body; (2) it promotes the conversion of bloodborne fuels to forms that can be stored: glucose to glycogen and fat and amino acids to proteins; and (3) it promotes the storage of glycogen in liver and muscle, fat in adipose tissue, and proteins in muscle (see Figure 12.2). In short, the function of insulin during the cephalic phase is to lower the levels of bloodborne fuels, primarily glucose, in anticipation of the impending influx; and its function dur- ing the absorptive phase is to minimize the increasing levels of bloodborne fuels by utilizing and storing them.
the fasting phase is characterized by high blood levels of glucagon and low levels of insulin. Without high levels of insulin, glucose has difficulty entering most body cells; thus, glucose stops being the body’s primary fuel. In effect, this saves the body’s glucose for the brain, because insulin is not required for glucose to enter most brain cells. The low levels of insulin also promote the conversion of glycogen and protein to glucose. (The conversion of protein to glucose is called gluconeogenesis.)
On the other hand, the high levels of fasting-phase glucagon promote the release of free fatty acids from adipose tissue and their use as the body’s primary fuel. The high glucagon levels also stimulate the conversion of free fatty acids to ketones, which are used by muscles as a source of energy during the fasting phase. After a prolonged period without food, however, the brain also starts to use ketones, thus further conserving the body’s resources of glucose.
different set point models for eating
- glucostatic theory (the idea being that we become hungry when our blood glucose levels drop significantly below their set point and that we become satiated when eat- ing returns our blood glucose levels to their set point.) –> meal initiation and termination (short term)
- lipstatic theory (every person has a set point for body fat, and deviations from this set point produce compensatory adjustments in the level of eating that return levels of body fat to their set point.) –> long term regulation
Thus, the dominant view in the 1950s was that eating is regulated by the interaction between two set-point systems: a short-term glucostatic system and a long-term lipostatic system.
PROBLEMS WITH SET-POINT THEORIES OF HUNGER AND EATING
- There is an epi- demic of overeating, which should not occur if eating is regulated by a set point.
- evolutionary
- high levels of fat deposits at the time of eating are associated with increased, rather than decreased, hunger
- set-point theories of hunger and eating are defi- cient because they fail to recognize the major influences on hunger and eating of such important factors as taste, learning, and social influences.
positive-incentive theory
humans and other animals are not normally driven to eat by internal energy deficits but are drawn to eat by the anticipated pleasure of eating—the anticipated pleasure of a behavior is called its positive-incentive value.
According to the positive- incentive perspective, it is the presence of good food, or the anticipation of it, that normally makes us hungry, not an energy deficit.
Unlike set- point theories, positive-incentive theories do not single out one factor as the major determinant of hunger and ignore the others. (taste, flavor, learned about food, glucose levels etc..)
PREMEAL HUNGER.
the strong, unpleasant feelings of hunger you may experience at mealtimes are not cries from your body for food; they are the sensations of your body’s preparations for the expected homeostasis-disturbing meal. Mealtime hunger is caused by the expectation of food, not by an energy deficit.
the body enters the cephalic phase and takes steps to soften the impact of the impending homeostasis-disturbing influx by releasing insulin into the blood and thus reducing blood glucose.
PAVLOVIAN CONDITIONING OF HUNGER
hunger is often caused by the expectation of food, not by an energy deficit.
SATIETY SIGNALS:
- volume of food
- nutritive density (kcal)
sham eating: wanneer ratten een buis hadden waardoor hun eten niet naar hun maag ging maar meten uit hun lichaam hadden de ratten nog steeds een verzadigingsgevoel, shameating geeft geen energie aan het lichaam want het gaat meteen eruit dus dit is bewijs tegen set point theorie, want dan zouden sham eaters heel veel moeten eten om die energie aan te vullen maar blijkbaar aten die raten even veel als mensen waarbij het eten wel naar de maag ging. na een aantal sham eating meals gingen ze wel meer eten
appetizer effect: nog een argument tegen set point theory of satiety, als je iets kleins eet voor een grotere maaltijd krijg je juist meer honger want het zorgt voor het beginnen van de cephalic phase
hoe groter de serving size hoe meer we eten
je eet ook meer als je met andere eet
- SENSORY-SPECIFIC SATIETY: cafeteria effect, als je een bepaald soort voedsel eet wordt de positive incentive value van dat voedsel laag en die van een ander wat hoger dan die van het voedsel wat je al eet, je satiety voor het voedsel wat je al eet wordt dus hoger maarje kan wel nog ander voedsel eten
voordelen: gevarieerd eten en veel eten op momenten dat het kan (komt van vroeger)
appetizer effect
nog een argument tegen set point theory of satiety, als je iets kleins eet voor een grotere maaltijd krijg je juist meer honger want het zorgt voor het beginnen van de cephalic phase
The Myth of Hypothalamic Hunger and Satiety Centers
vroeger:
-VMH, werd gezien als satiety center
- LH, werd gezien als feeding center
was onjuist maar:
bilaterale laesie VMH –> hyperphagia: overmatig eten + obesitas
- dynamic phase
- static phase
bilaterate laesie LH –> aphagia (complete stopzetteing van eten, dood. kan ook leiden tot adipsia (complete stopzetting van drinken)
theorie onjuist want:
- VMH is niet satiety center, overeten omdat ze aanomen niet omdat ze overeten.
bilaterate laesie verhoogt insuline, dat zorgt voor lipogenesis (productie lichaamsvet) en vermindert lipolysis (afbreken lichaamsvet).
- Veel effecten VMH laesie niet direct gevolg van schade VMH
Bij grote schade ook schade aan bundel axonen vanuit paraventricular nuclei: kernen in de hypothalamus die een rol spelen bij eten en synthese van hormonen > vrijgelaten door posterior pituitary
Schade aan bundel axonen of paracentricular nuclei > hyperphagia + gewichtstoename (net als VMH)
- LH niet ‘feeding center’
- Bilaterale laesie LH > ernstige motorische stoornissen + gebrek
gevoeligheid sensorische input (eten en drinken slechts 2 voorbeelden) LH geen centrum specifiek voor honger
Modern Research on the Role of Hypothalamic Nuclei in Hunger and Satiety
Recent onderzoek > bepaalde cel populaties in hypothalamus invloed op honger en satiety:
Neuronen in paraventricular nuclei > fungeren als voedingsstofsensoren >
invloed voeding en satiety
Neuronen in arcuate nucleus (kern in de hypothalamus met hoge
concentraties van leptine en insuline receptoren) > invloed metabolisme energiebronnen (geconsumeerd voedsel)
Centrum van neuraal netwerk dat integreert met receptoren in bloed en darmen
Role of the Gastrointestinal Tract in Satiety
Cannon & Washburn > theorie:
Honger is het gevoel van samentrekkingen veroorzaakt door een lege maag
Satiety is het gevoel van een opgezette maag
Echter: mensen zonder maag > esophagus direct verbonden met duodenum: het bovenste gedeelte van de intestine, waar de meeste glucose en aminozuren worden geabsorbeerd in het bloed > hadden wel honger- en satietygevoel + behoud lichaamsgewicht door meer maaltijden kleinere omvang
Nieuwe studie > gastrointestinal tract bron van satiety signalen
Transplantatie extra maag en darmlengte bij ratten > belangrijkste slagaders/aders implantaat verbonden bloedsomloop > voedsel in getransplanteerde maag + vastgehouden door een strop rond pylori sphincter > dalen zowel calorieën en volume voedselvoedselinname
Omdat getransplanteerde maag geen functionele zenuwen > gastrointestinal satiety signaal moest via bloed naar hersenen
Voedingsstoffen niet opgenomen vanuit maag > satiety signaal kan geen voedingsstof zijn
Dus: chemische stof vanuit maag als reactie op toename calorie en volume
