Learning and Unlearning Disease

In 1920, an American psychologist named John Watson set out to prove that all human behavior was learned, not inherited. He was convinced that he could mold anyone to do or be anything. And for some reason he chose to start this crusade of proof by terrorizing a nine month old child named Little Albert. Before this experiment little Albert had no fear at all of rats, but when Watson presented him with a white rat, just as baby Albert started reaching for it, he struck a steel bar with a hammer directly behind Albert's head. The baby cried and fell forward, his threat response triggered by the sound. You can actually watch videos of this experiment on YouTube. It’s…disturbing. Watson shows no emotion at all about the child’s distress. Then Watson repeated this experiment seven more times over two sessions. By the end of these seven exposures, Albert would cry and try to crawl away just from seeing the rat, without any noise at all. The fear association to white rats had been wired in.

Five days later, they found that Albert was now also afraid of a white rabbit he'd previously happily played with. Then he cried at a white dog, a fur coat, and even a Santa Claus mask. Watson's own white hair caused Albert to cry when he leaned in close. The fear of the white rat had generalized, causing baby Albert to be afraid of anything that looked similarly white and furry. His brain had taken one learned association and attributed it to anything that seemed remotely similar. Watson had only repeated this experiment seven times, and in that short time he had created a network of fear responses in Little Albert to an entire category of objects. Watson had proven that emotional responses could be created through simple association, and that you could wire fear to literally anything if you paired it with something scary.

Seven pairings. That's all it took to create a fear that spread to everything white and furry. And this is exactly the pattern we saw earlier with the asthma patients whose triggers kept multiplying - first cats, then dogs, then dust, then cold air, then exercise. Or the IBS patients whose safe foods kept shrinking. Medicine notes these expanding lists and thinks, yep, the disease is progressing as we expect it to. But the learning science is clear; the brain learns one association and then generalizes it to anything that seems similar. It's trying to protect you by casting a wide net - and once that net catches something, it becomes part of the pattern.

And like we showed in the last chapter with allergies and food sensitivities getting wired in through associations, they are also wired into threat, and the intermittent nature of them makes that even more sticky. When you're in threat, which by definition we likely are when we’re sick, you’re more hypervigilant. Which can lead to scanning for symptoms, which then trains your nervous system to detect smaller and smaller signals. The same synaptic strengthening that lets you learn a language or memorize facts is now making you better at feeling pain, or gut sensations, or whatever you're monitoring, just like any skill gets honed through practice and attention. Remember the monkeys in Merzenich’s experiment who were learning to touch a spinning disc? The region in their brain for that specific finger exploded, they actually grew more neuronal connections in that part of their brain to enhance their ability to perform that skill. The same thing is happening here. Signals that used to be too weak to reach conscious awareness now register loud and clear. Medicine sees this hypersensitivity and assumes it's causing the condition - but you weren't born with intestines that feel everything, or hypersensitive lungs.

Think about it this way. If you lived somewhere with tigers around every corner, you would get better and better at hearing specific crunching of leaves, or rustling in the bushes as threats. Your body would fire off the threat response earlier at smaller signals. The vigilance is a survival skill, and the sensitivity is a product of the vigilance, not the other way around. Your brain is training itself to feel more by paying so much attention. Which makes sense when it comes to monitoring for a tiger, but can become maladaptive when it’s keeping us in a feedback loop of threat and symptoms.

So now we’ve mapped how we can wire in illness patterns through learning and neuroplasticity. Luckily these same processes that get us sick and stuck can also be used intentionally to get us out. Let’s look at the other side and see how we can condition them out.

Unlearning responses

In the 1970-80s, Mark Bouton at the University of Vermont wanted to know if we could reverse the kind of conditioning that Watson did to Little Albert; if we could extinguish (get rid of) or undo that kind of fear response. So he first taught rats to be afraid of a specific tone by pairing it with a shock, similarly to how Watson paired the white rat with the loud noise. Then he played that same tone repeatedly without the shock until they stopped showing fear.

He showed that when he extinguished a fear completely in one location and then tested the animal in a different room, the fear was still there, as strong as ever. The animal hadn't unlearned that the tone was dangerous; it had only learned that the tone wasn’t dangerous in that specific room. So then he tried testing another assumption: he would extinguish a fear completely, and then he would wait a few weeks without any training or exposure, and do the test again. He found that the fear returned completely, as if the extinction had never happened, even in the learned location. And finally he showed that when he extinguished a fear, and then exposed the animal to mild stress that was completely unrelated to the original fear conditioning, the fear came roaring back. So what he was seeing was that extinction wasn't actually erasing anything, it was just temporarily being suppressed under specific conditions.

By the 1990s, brain imaging technology finally let researchers see what was actually happening during extinction, and it confirmed what Bouton's behavioral experiments suggested. When they looked at the brain activity during extinction, they found that the fear neurons in the amygdala still initially activated when the stimulus appeared. The amygdala was still recognizing "this is the thing that was dangerous," but for responses that have been extinguished, neurons in the prefrontal cortex would quickly activate and inhibit the fear response before it could fully develop into the physiological and behavioral fear reaction. Which makes a lot of sense. If you learn that snakes are dangerous, and then you experience some snakes in the wild that don’t attack you, you don’t want that fear circuit to disappear completely, you just want slightly more nuanced activation. Because some snakes ARE dangerous, and your brain needs to know that.

Contextual learning

If you study for a test when you’re tipsy, you’d be best served by being tipsy while you take the test too. In the 1960s researchers found that when people learned something while they were drunk, they could remember what they learned better when they were drunk again, rather than sober. And when they studied this weird discovery further, it turned out to be true for every state they tested. Information learned while anxious was best recalled during anxiety. Skills practiced while calm were most accessible when calm. Pain states, and mood states, and even specific body positions all created state-dependent memory networks that were most available when those states returned. And this understanding actually helps Bouton's findings make a lot more sense. The rat didn't learn 'the tone is safe now.' It learned 'the tone is safe in this room.' The safety learning was tagged to that specific context, which is why it disappeared the moment you changed the room. If you change the context, you change the learning. Which makes sense evolutionarily. Your body could learn, tigers can’t get me in this cave, but when I go outside all bets are off. We had to be able to make context dependent threat assessments, so we could let our body relax when it was safe, and could stay vigilant when the possibility of threat demanded it.

In the 1980s a researcher named Gordon Bower at Stanford hypnotized subjects to feel either happy or sad, then had them learn lists of words. Later, he tested their recall in either the same mood or the opposite mood. People who learned words while sad remembered them better when sad again. People who learned while happy recalled better when happy. The brain wasn't just storing the information; it was storing the information tagged with the internal state present during learning. This means that if you learn coping skills while feeling calm and safe in a therapist's office, these get neurologically tagged as "calm state" information, making them least accessible precisely when you need them most, during the stressed, symptomatic states where the maladaptive patterns live. It’s why meditation is often just like doing crossword puzzles. You are learning to be calm WHILE you meditate, in those specific circumstances. When you are annoyed with your spouse because they didn’t empty the dishwasher, that meditative state you’ve been practicing isn’t going to come up unless you make it come up. And both of these state dependent findings, mood states and state-dependent learning, provide a lot of context for how illness is self perpetuating. When you're sick, you're learning all your patterns in the sick state. Every symptom, every fear response, every coping attempt gets tagged to that pathostatic state. So being sick becomes the context that triggers being sick - your body learns to be a certain way when it's getting specific stimuli, and the symptoms and physiology that state creates actually create a feedback loop that becomes more and more sticky and thus chronic.

And just to round out how far these associative findings go, let’s look at the research on drug overdose as it relates to location. A researcher named Siegel showed that situation-specific drug tolerance is capable of preventing fatal overdoses. There was one man who received the same morphine dose four times a day for four weeks, always in his dimly lit bedroom, where he was bedridden. But one day he for some reason dragged himself out of his bedroom into the brightly lit living room. When his son gave him the exact same dose in the living room he died from an overdose. His body didn’t mount the tolerance response it had learned, without the context of the room it had learned it in. And if context can determine whether or not a morphine dose is fatal, imagine what it's doing to every other physiological process. Pain researchers discovered that chronic pain patients often felt better in novel environments like hospitals or vacation spots, only to have their pain return the moment they got home. The brain had learned not just "pain" but "pain in my bedroom," "pain at my desk," "pain at 3 PM," creating elaborate networks of association that turned entire environments into symptom triggers.

Two necessary components

In 2004, Phelps and colleagues looked at what was happening in the brain during fear extinction. What they found was that successful updates required two things firing simultaneously: the fear center, where the automatic threat response lives, and the prefrontal region responsible for conscious processing and safety learning. The prefrontal cortex forms the new 'this is safe' memory and actively inhibits the fear response, but only if the fear memory is active at the same time. The strength of connection between these two regions predicted how well the extinction stuck.

And for complex threat responses that have been encoded throughout many instances in your life, this can't just happen once. You need the new integrated experience to happen across contexts just like the fear learning did. Across different moods and times of day and situations, in the actual moments where life activates the old pattern. Each time you meet the activation with both systems online, feeling it while staying present, you're building the new wiring in that specific context. Do it enough times, in enough different situations, and the new pattern starts to become the default.

Just as symptom expression gets encoded into our brain in the same way we learn how to play piano, the same system can also be used to update the threat response feedback loop that is causing learned symptoms and disease expressions.

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We now have the science showing how disease patterns wire in, and the science showing how to update them. Combined with what we've learned about what's driving pathostasis in the first place, for the first time we can see both sides of the problem, and what we can do about it.