If an individual is addicted to a thing and another individual is addicted to an event, but would not feel anything if there is a change from what they are addicted to — even if the addiction to others — is it all dopamine?
There is a recent [August 5, 2025] spotlight by Stanford Medicine, Why our brains are wired for addiction: What the science says, stating that, “For millennia, human survival depended on the drive to seek out pleasure and avoid pain. When we do something beneficial — like eating when hungry or seeking shelter when cold — our brain releases dopamine, a chemical messenger that makes us feel good and reinforces the behavior. This system worked beautifully in environments of scarcity. Pursuing things that released dopamine was, indeed, more important than anything else.”
“In modern times, however, humans have become inundated with easy access to things that light up this reward pathway in the brain: sugary and salty food, nicotine, alcohol, drugs, slot machines, and digital media, among others. All are engineered to deliver a faster, more intense dopamine spike than anything in nature.”
“Some people are more vulnerable to addiction than others. Genetics account for roughly 50% to 60% of the risk, according to family and twin studies. Traits like impulsivity, emotional dysregulation, and certain mental health conditions — including attention deficit/hyperactivity disorder and bipolar disorder — also increase susceptibility.”
Dopamine
What is the mechanism for the experience of reward in the brain? If empirical evidence shows that the reward pathway in the brain is active for reward or that dopamine spikes, what is a model of addiction that can be used to show why there is sometimes helplessness in cases of addiction?
If an area of the brain is active during an experience, is it just one chemical signal [or neurotransmitter] that is involved? Neuroscience has established that glutamate is a major excitatory neurotransmitter, so for the neurons in the reward pathway, is it just dopamine that overtakes, or is there a collaboration [of other neurotransmitters] in a cluster of neurons? Also, when neurons are active, electrical signals are also at work, so does this mean that there are no roles for electrical signals in addictions at all? Sometimes, too, even without addiction, there could be dopamine release, but no experience of reward or pleasure; how come? Simply, what is the combination for reward, since dopamine alone, even if [say] induced, has not solved all addictions.
The reward pathway is lit during addictions — so to speak — but how does information get there, given that there is a myriad of addictions for different people? Say, information arrives by electrical signals, could there be a configuration or intensity it arrives with, for an addictive thing for one person or an addictive event for another person, to result in the release of dopamine? Is dopamine for attention in the reward experience, or is it the configuration for the completion of reward? What does dopamine do for reward experience, since it is also implicated in several non-reward functions?
In seeking answers about how to properly model addictions, it is already too cheap to just throw dopamine around, given that, directly, there could be other chemical signals as well as electrical signals. Neuroscience has established that one neuron has around 6,000 to 10,000 synapses. This means that even the so-called dopamine neurons project axon terminals and have their dendrites connected to other axons as well.
Modeling Addiction
To develop a standard model for addiction, the candidates are electrical and chemical signals of neurons. This means that if someone is addicted to a thing, that thing has a configuration that consists, conceptually, of electrical and chemical signals. Then the thing also has a sequence or route that goes [say] to the reward pathway [also mechanized by electrical and chemical signals]. This is plausible because something [or the thing] has to get to the reward pathway, to prompt activation, conceptually.
Also, since reward is possible for some non-addictive situations, like some surprises, and so on, it could mean that there are sometimes attempts that get to the reward area that result in reward, but sometimes, some don’t, even in cases like learning. So, for reward, there are several attempts and something attains [a configuration or an attribute like attention or prioritization] and works.
What gets there are electrical signals, coming off chemical signals, in sets. Signals are theorized to work in sets in clusters of neurons. So, the configuration for functions are electrical and chemical signals in sets. This includes for reward. In sets, electrical and chemical signals interact to result in functions. They also have states that become the extent to which the interactions proceed. Electrical signals, in a set, split, conceptually, with some going for early interactions. This split is postulated because of saltatory conduction, where some electrical signals leap, in myelinated axons, going faster. Splits explain the mechanism for what is labeled predictive coding, processing, and prediction error.
This refutes what is called reward prediction error, because there is no mechanism for that in the brain.
How do electrical and chemical signals in a set drive addiction, by their splits, sequences, thick sets, intensities, and so forth? How does this explain what a substance does and what an object does, how does it model what it looks like in the brain, not just the simplicity of dopamine? Also, with genetics, how are there aberrations for several other offspring?
The evidence is with electrical and chemical signals in sets.
There is a recent [August 8, 2025] essay in Vogue, The Easiest Way to Generate Dopamine, According to Neuroscience, stating that, “As it turns out, the simple act of smiling is one of the most effective ways to generate dopamine and lower the stress hormone cortisol.”
This article was written for WHN by David Stephen, who currently does research in conceptual brain science with a focus on the electrical and chemical signals for how they mechanize the human mind, with implications for mental health, disorders, neurotechnology, consciousness, learning, artificial intelligence, and nurture. He was a visiting scholar in medical entomology at the University of Illinois at Urbana-Champaign, IL. He did computer vision research at Rovira i Virgili University, Tarragona.
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