🎯 Objectives
To familiarize the students with the:
- Brain and motivational states 🧠🎭
- Homeostasis ⚖️, include temperature regulation 🌡️, Cellular and brain controls of Thirst 💧, Reward systems and addictions 🎁, Fear 😨, aggression 😡, attachment ❤️
- Hunger 🍽️, Body weight set point (Theories) 📊, Obesity 🍔, Anorexia Nervosa 🚫, thirst 💧, bio-rhythms ⏰, Sleep and awakening 😴⏰
- Pathology related to sleep cycles ⚠️
- Sleep disorders and treatment 🩺
- Neurophysiology and biorhythms 🧬⏰, Sleep and awakening cycles 😴🌅, Dreams 💭, Sleep disorders 😴⚠️
🍽️ Factors that Control Food Intake Behaviors (continued)
In the last lesson we have discussed the contribution of the oral factors 👄, (palatability etc.) and the smell 👃 and sight 👁️ of food, cognitive 🧠 and learning influences on what we eat and how we eat. Now we will find out if the gastric factors 🫃 (stomach, the alimentary canal, the digestive system), contribute to feeding behaviors 🍴.
🫃 Gastric Factors
Gastric factors: The gastrointestinal tract is important in digestion and breaking down of food into nutrients needed by the body 🧬. The stomach seems important intuitively because we eat when the stomach is empty 🫃⭕ and stop eating only when there is feeling of fullness in stomach 🫃🔵. But this is not true! ❌
🧪 Cannon and Washburn (1912) Study
Let's find out through the evidence from experiments carried out to isolate the stomach factors 🔬.
If the feeling of fullness comes from the stomach as a signal to stop eating 🛑, what if we preload the stomach in some way, and the stomach is distended or expanded (remember that the stomach has the capacity to flex and contract 🫃↔️)?
The first experiment of balloon preloading of the stomach 🎈 was carried out by Cannon and Washburn (1912 cf Pinel 2002) 👨🔬, Cannon was the experimenter and Washburn the subject, he had to swallow the balloon 🎈👄) and reported whenever hunger pangs felt 😣. As he reported the pangs Cannon measured electrical activity of stomach contractions through a mechanism placed beforehand ⚡🫃.
The hunger pangs were found to be correlated to stomach contractions 📊, leading to the view that stomach was important in hunger control 🫃🎯. When there is preloading of the stomach with water 💧 or some other substance, there is decrease in food intake ⬇️🍽️.
🚫 Evidence Against Stomach Control
But this theory was not supported by the following ❌:
1. The stomach is almost always full 🫃🔵; it is never completely empty except in long fasting or starvation 🚫🍽️.
2. When we are full and have eaten enough 🫃✅, if required or asked to eat even on a full stomach we can add some more good food (think of the Pakistani hospitality! 🇵🇰🍛).
3. In human patients when the denervation or removal of stomach takes place 🏥🫃 and the esophagus is connected directly to the duodenum 🔄, they still report pangs of hunger and feelings of being full 😣, and continued to eat to maintain their body weight ⚖️, although their meals were smaller 🍽️⬇️. This is similarly true of animals as well 🐀.
🩸 Koopmans (1981) Blood Vessel Experiment
However, Koopmans (in 1981) 👨🔬 carried out an experiment on animals where he attached another stomach 🫃➕🫃 and connected the blood vessels through the additional stomach 🩸. In this procedure, the food was passed from the additional stomach to the real stomach (measured) 📊, but blood vessels only passed through the new stomach 🩸🔄--- interestingly the animals stopped eating in response to some signal from the blood 🛑🩸.
It appears that there must be some chemicals not found in the food 🧪, but which stimulated signals for stopping of eating 🛑.
⏱️ Timing of Satiety
Keeping this evidence and the fact that one stops eating even before the process of digestion and absorption of food starts taking place ⏰ (as this requires time ⏳), there appears to be some role for gastric cues 🫃📡. Feeding ends even before the nutrient-deficiency signals are terminated ⏱️, therefore there has to be another signal to terminate feeding 🛑, coming from the gastric region 🫃.
🧪 Gut Peptides - CCK
Smith, Gibbs and Young in their studies (from 1973-1976 onwards 👨🔬) suggest that there may be peptides (short amino acid chains 🧬) i.e., hormones 💉 or neurotransmitters 🧪 which signal the satiety signal 🛑.
The ingested food may be triggering the release of hormones into the bloodstream 🩸. One of these gut peptides cholecystokinin (CCK) 🧪 when injected led to rats eating smaller meals 🐀🍽️⬇️- or inhibit feeding without causing any illness or pain 🛑😊.
Administration of this peptide directly into the brain 🧠💉 is not as effective as injection into the blood stream 🩸💉. However, later studies by Mineka and Snowdon (1978) 👨🔬 have shown that this effect does not last very long ⏱️—therefore there are other controlling factors for food intake 🍽️🎛️.
🔥 Metabolic Factors
Thus, we have found out that the oral 👄 and gastric 🫃 are important in feeding but not enough ⚠️, therefore we now look at the metabolic, energy and neural controls 🧬⚡🧠 to see if those are important in the initiation and termination of feeding signals 🍽️.
🍬 Blood Glucose Levels
Metabolic Factors: If Glucose level in the blood decreases 🍬⬇️ it leads to initiation of eating ▶️🍽️, increases in blood glucose 🍬⬆️ would lead to cessation of eating 🛑.
More recently Campfield and Smith (1990) 👨🔬 have shown that rats with free access to food and water 🐀🍽️💧 were monitored for blood glucose through a catheter 💉. These rats had constant level of blood glucose at about 2% 📊, but just before eating, the blood glucose levels dropped to about 8% ⬇️, indicating that blood glucose levels may be a signal for food intake 📡🍽️.
🎯 Set Point Mechanisms
This takes us to the now classic assumption of set points in the body of glucose 🍬 and of lipids 🧈. The set point means that there is an energy set point ⚡🎯 which determines how much is eaten and when ⏰🍽️.
This has three basic components:
- The set point mechanism 🎯 (assumption is that these are neuronal receptors 🧠)
- The detector mechanisms 📡 (which detect differences from the set point ⚖️)
- The effector mechanisms 🔧 which are to bring about a change so that the set point level is met ✅
Thus, there is a set point for glucose levels 🍬, a set point for fat levels 🧈, a set point for weight ⚖️ etc. We will discuss the theories which propose the first two 1️⃣2️⃣.
📊 Glucostatic Theory
Glucostatic Theory proposed by Mayer: 👨🔬 This theory suggests that feeding regulatory system is actually keeping the glucose set point in the blood at a constant level 🍬⚖️. There are glucostatic set point monitors 📡. Gluco-receptors in the hypothalamus 🧠🏥 constantly gauge the level of glucose in the blood 🍬🩸. This is a short-term mechanism ⏱️ for initiation and cessation of feeding 🍽️.
💉 Glucose and Insulin Effects
If the glucose levels in the blood fall 🍬⬇️, then the glucose from pancreas is released in blood stream 🏥🩸 leads to an increase in eating ⬆️🍽️, glucagon injection 💉 led to decreased eating ⬇️🍽️ and reduced stomach contractions 🫃⬇️.
Further, Insulin injections 💉 lead to marked hypoglycemia (reduced glucose levels in the blood 🍬⬇️🩸). This led to increased eating ⬆️🍽️ as insulin increases the entrance of blood glucose into the cells 🍬➡️🧬.
🍬 Sugar Type Experiments
In an experiment, this injection was followed by 💉:
a) Glucose injection 🍬💉
b) Fructose or mannose 🍯 (types of sugars: fructose cannot cross blood brain barrier ❌🧠 but can be utilized by the liver 🫀, mannose can be used by both brain 🧠 and liver 🫀) or ketone bodies (fuel used by the brain 🧠 not the liver 🫀).
All animals given some nutrient after the insulin injections showed a drop in feeding ⬇️🍽️, indicating that it is not the brain signals 🧠❌ but some controls of the periphery 🔄 which monitor feeding 📡.
🧈 Lipostatic Theory
Lipostatic Theory: Lipostatic theory states that there is a body set point for lipids 🧈🎯 and any deviation decrease in the body stores of fats ⬇️ would lead to initiation of feeding ▶️🍽️. This is long term mechanism ⏰ body weight maintenance ⚖️.
(Remember in cases of starvation 🚫🍽️, stored body fats are broken down for providing glucose 🧈➡️🍬).
🤔 Difficulties with Set Point Theories
The difficulties with the set point theories are ⚠️:
a) That these are not consistent with the evolutionary perspective 🧬🌍--- when man didn't know if he would be able to eat next 🤷— (if hunt successful only then food would be available right? 🏹🦌), how is possible to have a set point sending out signals to regulate food 🎯❓.
b) Hunger and feeding are not just following glucose patterns 🍬📊, people around the world have culturally varied food patterns 🌍🍛. How can this be explained in glucostatic or lipostatic theory? 🤔❓
🧠 Neural Control of Feeding
Research into the neural controls of hunger has been ongoing since the 1940's 🔬📅. There are two brain areas the Ventromedial Hypothalamus (VMH) 🏥 and the Lateral Hypothalamus (LH) 🏥 which have become more important from the 1940's- 1980's 📅.
Hypothalamus is important in eating and drinking 🧠🍽️💧. We know hypothalamus is important in motivational and survival behaviors 🎭🛡️. If there would be no hypothalamus 🚫🧠 there would be no feeding, and no drinking controls 🚫🍽️💧. There is specialization within hypothalamus where each region works in coordination with the bodily needs, and other regions 🎛️.
🫃 Ventromedial Hypothalamus (VMH)
Ventromedial Hypothalamic damaged rats become obese rats 🐀➡️🐀📈. This was first demonstrated by Anand and Brobeck in 1943! 👨🔬 VMH lesions to hyperphagia (overeating 🍽️⬆️), and LH lesions lead to aphagia (no eating 🚫🍽️). These have been shown to be the same effect in rats 🐀, dogs 🐕 and monkey 🐵—also humans 👨. The following are the similarities in VMH rats and human 📊:
1️⃣ Food Nutritive Content Challenge
If the nutritive content in food is decreased ⬇️🥗 then the normal would increase food intake to compensate ⬆️🍽️ but VMH are finicky eaters 🐀🚫. The VMH cannot respond to these challenges ❌⚠️.
2️⃣ Palatability
Palatability is important for VMH rats and humans 😋🎨. If we increase the palatability, it leads to increased eating in VMH animals and human ⬆️🍽️, whereas normal stop eating in response to body's signals 🛑📡 (The VMH become obese as a consequence 🐀📈).
3️⃣ Work for Food
If effort is involved to work for food 💪🍽️, the VMH damaged rats and fat humans would do minimal work for food ⬇️. In an experiment, normal and VMH animals and fat humans were given peeled and unpeeled almonds 🥜. Fat humans and the VMH rats ate more unpeeled 🥜 whereas the normal ate about 50% of the peeled and unpeeled almonds ⚖️.
🛑 VMH as Satiety Control
There is a hypothesis that VMH may be the satiety control 🛑🎯 these areas controls the signals for stopping of feeding 🚫🍽️- which is why if VMH is damaged ⚠️ the inhibition is gone 🚫, and the animals continue eating! 🍽️🍽️🍽️
🚫 Lateral Hypothalamus (LH)
LH damaged animals are starving rats 🐀🚫🍽️. These animals are aphagic (do not eat 🚫🍽️), adipsic (do not drink water 🚫💧) if they are not tube fed, they die 💀. Recovery is slow and takes place in phases ⏱️.
🔄 Recovery Phases
These animals can recover eating but not drinking 🍽️✅💧❌. Eventually they start drinking condensed milk 🥛 but no water 💧❌. Their recovery reaches almost normal levels of eating 🍽️⚖️, but these animals cannot respond to challenges ⚠️. The LH animals also cannot eat to compensate for initial weight loss 🐀⬇️⚖️. These animals cannot fully recover their normal weight ⚖️⬇️.
▶️ LH as Initiation Center
It is said that the LH is the center for initiation of eating ▶️🍽️ which is why lesions lead to the starvation like state 🚫🍽️ (no LH no signals to eat ❌). However, it is difficult to interpret as many NTs passing through it 🧪, NE 🧠 DA 🧬 may also be involved ⚙️.
It is Possible that this damage causes motivational deficit/inertia that animals don't want to eat or drink 🚫🎭. This is supported by the fact that there is no spontaneous activity of these animals 🐀❌⚡. Further there is sensory neglect (lack of response to visual 👁️❌. Tactile 🤚❌ and other stimulus 🔊❌).
🧪 Neurotransmitters and Hormones
Other factors such as Neurotransmitters and hormones have also been found to be important 🧪💉:
• The role of Norepinephrine 🧪 has been highlighted by studies by Liebowitz and her colleagues especially in the area of LH as stimulation of NE rich neurons leads to initiation of eating ▶️🍽️.
• More recently role of gut peptides 🫃🧪 has also emerged as important, in the initiation and controlling feeding 🍽️🎛️.
• We have already studied that there is a large amount of serotonin in the gut 🫃🧪. There appears to be role for the chemical in the signals for feeding 🍽️📡.
📚 References
- Carlson, N. R. (2005). Foundations of physiological psychology. Pearson Education New Zealand.
- Pinel, J. P. (2003). Biopsychology. (5th ed). Allyn & Bacon Singapore.
- Bloom, F., Nelson., & Lazerson. (2001), Behavioral Neuroscience: Brain, Mind and Behaviors. (3rd ed). Worth Publishers New York
- Bridgeman, B. (1988). The Biology of Behavior and Mind. John Wiley & Sons, New York
- Brown, T.S. & Wallace, P.S. (1980). Physiological Psychology. Academic Press, New York
- Mogensen, G. J. (1977). The Neurobiology of Behavior. Lawrence Erlbaum Associates