Bill’s chapter on emotion in B:CP (omitted in the first 1973 edition) proposes that emotions are derived from somatic sensations and interconnections between the behavioral control hierarchy and “a second hierarchy of control … concerned with the sensing and control of quantities derived from sensors and … chemical messengers throughout the body” (B:CP 258-259). “An emotion is the combination of a goal and a feeling. […] one must select a goal, and feel the physiological state, and have the action blocked , before the state would truly be called emotional” (B:CP 256).
Here is a late manuscript by Bill Powers which presents a new version of the model:
Are feelings of pleasure, satisfaction, joy, and happiness considered to be emotional states. If so, it is hard to believe that these states are the result of “having an action blocked” which the previous post and Powers (B:CP, 2005, p, 256) indicate is required “before the state would truly be called emotional.”
If positive emotions such as happiness exist, they seem to be a result of goals/references being achieved rather than being blocked.
In short, it seems as if the Powers chapter on emotions is focused on negative emotions and ignores positive emotions.
Bill’s model says that perceptions in the somatic branch of the hierarchy are important inputs to the higher-level perceptions that we call emotions. His account emphasizes the role of conflict in producing those somatic sensations. However, nothing in the model precludes sensations arising in the course of successful control (or otherwise, but without conflict) and such sensations being input for perception of other kinds of emotions.
The emphasis on conflict and the ‘bad feelings’ that can result (but do not necessarily result) was probably a reflection of our general emphasis on understanding conflict in general.
I think Bill’s PCT model of emotion is consisent with the results of the Shacter-Singer experiment and their Two Factor Model that they proposed to explain the results thereof (Shacter & Singer, 1962). In their experiment, subjects were injected with epinephrine, which causes a feeling of arousal. They were then seated in a waiting area where another “subject” (a confederate of the experimenters) acted either angry or euphoric. When taken into the test lab and asked how they felt most subjects reported feeling the way the confederate acted. So the same kind of arousal can be cogntively “felt” as a bad (anger) or good (euphoria) emotion.
Arousal of the type produced by epinephrine is associated with “loss of control”, which can be the result of conflict but also persistent, difficult to overcome disturbance (such as that produced when the hot tamale at the costume ball happens to be a Capulet and you are a Montigue; in that case you might interpret the arousal as love).
When you are “in control” there are no arousal producing hormones, like epinephrine, being secreted so there is no somatic arousal to be perceived and “felt” cognitively. So being in control feels like no emotion – or something I would describe as being in the groove-- which is cerainly a good feeling but not the kind of good you feel when you meet the love of your life or win a debate about PCT (only the first of which I’ve actually experienced).
Epinephrine is both a hormone (adrenaline) and the most widely effective excitatory neurochemical, and gamma-aminobutyric acid (GABA) is the most widely effective inhibitory neurochemical, but at any moment there are dozens of neurotransmitters active in the nervous system.
“Gu et al. introduced three core affects: happiness, sadness, and stress, which are subsided respectively by three neuromodulators: dopamine, serotonin, and norepinephrine.” Editorial: Neurotransmitters and Emotions
Dopamine is associated with transient feelings of pleasure; serotonin, with more durative feelings of happiness or well-being.
The limbic system controls the relative concentrations of neurochemicals throughout the body, including within the brain. This is how its rapid association of present input and memory establishes the emotional tone of a situation before higher cognitive functions suss it out. Since it does this without conscious awareness, an experience of being in control is often somewhat (or entirely) illusory. Paying attention to corporeal sensations as they arise is an effective way clear of this.
GABA and 5-hydroxytryptophan (5-HTP) are excellent help for insomnia, by the way. The essential amino acid tryptophan is converted to 5-HTP in the brain, whence there are two repositories, one in the brain and one in the blood. The majority of serotonin in the body comes from 5-HTP in the gut.
If this were true (and given my considerable experience with psychoactive chemicals --hey, it was the 60s --I believe it’s possible that it is) then it would certainly contradict the PCT and Schacter/Singer models of emotion as well as the behavioral data of Schacter/Singer. In both the models and the experiment, the same drug – epinephrine – results in different emotions – euphoria or anger – depending on the context in which it is taken.
Are you saying that there are systems in the limbic system that control the relative concentrations of neurochemicals as the means of developing rapid associations of present input and memory? And that this has something to do with the sense of being in control being sometimes illusory? But paying attention to corporeal sensations as they arise is an effective way clear dispel the illusory sense of control?
What is the relationship between a sense of control and being in control, by the way? They talked a lot about a “sense of control” in that Nova program on the brain but they never talked about “being in control”, which, of course, is what PCT is all about.
Well, I agree with you there! I don’t have insomnia but I got a Rx of GABApentin for pain and I was always asleep 10 minutes after getting into bed.
Part of the confusion here is because norepinephrine is both a hormone (adrenaline) and a neurotransmitter, and because the research you are citing did not measure concurrent levels of dopamine and serotonin. Blunt instrument.
Gu et al calling ‘stress’ an emotion seems peculiar. It is what Bill and others called ‘arousal’, i.e. preparedness for action. This ‘arousal’ may be distressful, as in stage fright, or it may be pleasant excitement, as in ‘performance energy’, to recite a common example.
Further confusion is because these three substances also have other effects in the body (i.e. participate in other control loops).
Yet further, those effects, including the ‘arousal’ by epinephrine may be perceived as intensities and sensations which are ambiguous or neutral in respect to emotion in just the way that ‘arousal’ may be input to a perception called anxiety or a perception called excitement.
Finally, the availabilities of these are interlinked. Dopamine (which is derived from ) is the precursor to norepinephrine and epinephrine. (The amino acid tyrosine is a precursor of dopamine, epinephrine, thyroid hormones, and melanin.)
Yes, Sarah was taking Gabapentin for a while, then didn’t like it, but she’s fine with GABA. Gabapentin is an analog of GABA (by adding something to the molecule). Apparently it doesn’t hit all the same receptors as GABA, but it does have a similar calming effect. GABA is cheap and safe, why bother? Cynically, I may suppose that it has the virtue of a patent. (That’s why there’s no research on the extraordinary benefits of physiologic doses of cortisol.)
the same drug – epinephrine – results in different emotions – euphoria or anger – depending on the context in which it is taken.
Part of the confusion here is because norepinephrine is both a hormone (adrenaline) and a neurotransmitter, and because the research you are citing did not measure concurrent levels of dopamine and serotonin. Blunt instrument.
If the different levels of these chemicals were measured and found to be associated with the different emotions reported it would be evidence against the PCT model of emotion.
Gu et al calling ‘stress’ an emotion seems peculiar. It is what Bill and others called ‘arousal’, i.e. preparedness for action. This ‘arousal’ may be distressful, as in stage fright, or it may be pleasant excitement, as in ‘performance energy’, to recite a common example.
That’s the PCT model; same perception of arousal leads to different emotions depending on cognitive interpretation of the reason for the arousal. This contradicts Gu et Alaia who purportedly found that different neurochemicals are the cause of different emotions. Again, if Gu et Alaia are right, PCT is wrong (about emotion). Which is fine; it would just require revision of the PCT model of emotion.
My only complaint about your post is that you presented the Gu et al results as though they supported the PCT model of emotion. If you described them correctly then they don’t.
Yes, I agree, Rick. Though I would think of it as a generalization of the original proposal.
There’s actually no contradiction, Rick. Arousal due to epinephrine/adrenaline is associated with a subset of emotions. Still true. It’s just that other things are also true. To generalize the model to encompass the full range of emotions and somatic perceptions (‘feelings’) is not difficult. The same parts of the brain send signals down the brainstem and the resulting changes in somatic conditions may be perceived.
However to flesh out the proposal does not look simple. The neuropeptides also effect synapses more immediately. Our understanding of all these effects is too foggy still. Too much serotonin has effects that could possibly be confused with those of epinephrine (irritability, agitation, restlessness, anxiety, tremors, shivering, tachycardia etc.). A person with elevated dopamine can be competitive and aggressive with poor impulse control or the appearance of ADHD.
In the Schacter/Singer experiment the “set” of emotions (resulting from exactly the same somatic experience) went from anger to euphoria. Hu et al found that different somatic experiences are associated with this same set of emotions. So I think the contradiction between the PCT model of emotion, which is consistent with the Schacter/Singer behavioral results, and the Hu et al model, which is not, still seems pretty huge.
The hugeness of difference is in the data about correlation of the other neurotransmitters with differences in interpretation as emotion. Schacter and Singer having zero data is as huge a difference as they could have.
In the Schacter and Singer study, subjects in the “euphoric model” (EM) condition received *exactly the same endogenous neurochemicals * as those in the “angry model” (AM) condition. Thus, it is highly unlikely that subjects in the EM condition would just by chance happen to have had more of the Hu et al “happiness” endogenous neurochemicals in their system than those in the AM condition and that those in the AM condition would just by chance happen to have had more of the Hu et al “anger” endogenous neurochemicals in their system than those in the EM condition. But that is what would have to have happened if Hu et al are right about the differnet endogenous neurochemicals being the cause of the differnet emotions.
In the unlikely event that such a confound exsted in the Schacter/ Singer study, making it all the more likely that Hu et al are correct about differnet endogenous neurochemicals being the cause of the different emotions reported by the subjects in the Schacter/Singer study, that would definitely put a nail in the coffin of the PCT nodel of emotion.
Calling them drugs limits the view to what has been administered by the experimenters. But they are endogenous neurochemicals with levels (and availabilities for adding to circulation) which are endogenously determined idiosyncratically in each individual. The conditions for that are unknown to us and were not considered in the Schacther/Singer study, nor are they considered in Bill’s proposal of a PCT model of emotion.
I have edited my post and changed all references to “drugs” to “endogenous neurochemicals”. I hope this makes it clear that the results of the Shacter/Singer study are incompatable with those of the Hu et al study. The only way I can see them being compatible is to assume that the presence of the “euphoric model” causes an increase in secretion of the endogenous neurochemicals that Hu et al found to be associated with happiness and that the presense of the “angry model” causes an increase in secretion of the endogenous neurochemicals that Hu et al found to be associated with anger. This is a bit too S-R for my taste but it would account for the incompatibility of the Schacter/Singer and Hu et al results.
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