Tag Archives: reduction

Causes, Facts, and Heroin

The lecturer moved his laser-pointer quickly over the loop of neural circuitry. He explained the role of Mu receptors in activating the circuit, which sent a signal round and round and came out as the behavior pattern we call addiction. It was all very neat.

It was so neat the he could have simplified his diagram by replacing the pretty brain graphic with a switch. Off would be synonymous with no addictive behavior. On would equal addictive behavior. If you took the theory, “Addiction = Brain Circuitry” at face value, anything that flips the switch would cause addiction. Yet we know that that situation does not obtain. Heroin flips the switch, but not everyone who takes heroin manifests addictive behavior.

For the advocate of “Addiction = Brain Circuitry”, there are two ways out of this dilemma. First, he can posit a multiplicity of switches. In other words, he can claim that there is an intervening network of necessary, but not sufficient, switches on either side of the Big Switch, mediating the input and output of the addiction circuit. But then in principle, all those switches could also be replaced with a single switch, and you are right back where you started. No limited set of if/then statements will be completely determinative.

The second way out of the non-correspondence dilemma is to simply abandon a complete and transparent explanation, in favor of reliable facts. Neurons are necessary to behaviors, and we know that because, if we zap certain neurons, we can reliably alter corresponding behaviors. That doesn’t exactly explain the behavior, but it lets us move on to knowledge of neural circuits and the experiences which correspond with changing the configurations of those circuits.

One might denigrate the second solution as an abandonment of truth-seeking. Perhaps, but that is not so bad, on a proper notion of truth. In solution #2, you get a theory, which is a set of reliable facts. To get to the truth what you need is an explanatory reduction. In other words, all the switches and their positions for a specific moment of behavior, across the cosmic board. Such an array is purely didactic. It refers to no knowledge, for it cannot reliably correspond with anything. You may think you know something about it, but you don’t – not until you begin to formulate a theory regarding it.

Johnnie shoots a dose of heroin because he has inherited a susceptible set of receptors, because he contains the dendritic representations of certain permissive life-lessons, because he lacks certain inhibitory representations, because he lives in a society which has heroin, because he anticipates certain effects from heroin injections. And on, and on, and on…

At the end of such an exposition (if there even is an end) what we have is just a snap-shot which we have pre-labeled, “Johnnie’s Addiction”. To make any sense of it – to know anything at all about it – we must delve in to the insufficient necessities, and be satisfied with their mere reliability. When we give Johnnie a medicine for his Addiction, we should expect that it will, to some extent, extinguish the behavior. We should expect that if we take away his heroin, his behavior will, to some extent, change. And in fact, our theory does correspond with the facts which it predicts, and upon which rests.

Like the addiction lecturer, we all frequently feel dissatisfied with reliability. We would like some non-provisional knowledge. Give us some truth, please. Aspiring to truth gets us nowhere, though. Truth is too hefty. To riff on Gettier’s classic thought experiment, Smith has the truth when he observes that a person with 10 coins in his pocket will get the job, once Smith sees that a person with 10 coins in his pocket gets the job. Yet he has no knowledge thereby. He cannot be (provisionally) right or wrong in such a statement, any more than a snapshot can be right or wrong (though our subsequent interpretations – theories – of the snapshot may be).

If Smith says, at his next interview, that the person with 10 coins in his pocket will get the job, and he takes care to put 10 coins in his own pocket in hopes of getting the job, then he may know something. He is making a knowledge claim regarding his experience with coins and interviews, and his claim may or may not correspond with his theory’s fact-conditions. Reliability is what he will get, and he will be happy with it, or not, as will we all.

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The Problem with Pain

My gaze swung between the man on the exam table and the radiograph displayed on the lightbox. He must have sensed a problem.

“What?” he asked.

What indeed. The film basically showed his shoulder blade broken in two.

“When did this happen?” I inquired. He had already told me once; I just needed to be sure that I’d heard it correctly.

“Yesterday afternoon,” he said, ” right after lunch.”

“And why did you wait until this afternoon to come in?’

“Well, I’m here mostly to get my wife off my back. If it was up to me, I wouldn’t have come in, but she thought it might be serious or something, because I tossed and turned last night.”

“Well,” I told him, “It is not a surgical problem, but it is a bad injury. You got lucky.”

After a moment’s reflection I added, “Didn’t that hurt?”

“Kind of,” he laughed, “But it eased up pretty quick.”

“Do you need any pain medication?” I asked.

“Oh, no,” he demurred, “Tylenol is doing fine for it.”

After a few more pleasantries, the man got up, walked out of my office, got in his car and drove back to work. Watching him wince slightly as he turned out of the parking lot, I couldn’t help but think of the patient before him – a fellow with no history of serious injury, a normal MRI of the lumbar spine, and disabling back pain.

The man with the back pain had wanted pain medication. I’d had to talk him out of it, which was a difficult task in that era. Because it was the era before the opioid crisis, when we were in the midst of a pain crisis, according to the medical authorities. Clinicians were directed to take everyone’s pain level the same way that we took their temperature, and to treat the abnormalities discovered by our measurements.

For those with eyes to see, the notion behind pathologizing pain was misguided, at least. The whole scheme rested on the idea that pain was simply activity in the neuronal substrate. Change the activity pattern, by activating opiate receptors, for example, and you get rid of the pain.

I am not being very charitable in my description, but I am being as charitable as I need to be. There are more nuanced depictions, which leaven the mix with talk of psychological context and so on, but the same suppressed premise lurks beneath them all. It is this: a chain of causal events ‘add up’ to pain, and that is just what pain is. X+Y+Z = Pain. But the necessity of such arithmetic has been in doubt even before Hume laid its troubles out so nicely for us Westerners.

Breaking down a phenomenon gives you its pieces, but does not grant commutativity. Activating opiate receptors does not reshape their owner’s pain experience according to a fixed script. Receptor activity is part of the description of a painful experience, along with psychological context, and personal history. Yet there is no prior necessity – necessity by law, rather than necessity in fact. We did not make the distinction.

Secure in our estimation of the relationship between the neuronal substrate and the pain experience, we went after opiate receptors like we go after splinters. Our efforts did not force anyone’s pain experience into a box, but we gave everyone who we treated a new pain experience. Sometimes it suited them better; sometimes it suited them worse. Many, many times it settled in the center of their psyches and they fell into orbit around it.

Our engagement with the epidemic of untreated pain predictably ended in chaos. Now we need to extricate ourselves, and what do we turn to but the tool already in hand.

Instead of the reduction to type, we have rebuilt our story of pain, revising our reduction on the basis of the same mistake. Receptors pertain to behaviors – in the neuronal substrate, and so in the psychology, and so in the organism – but pain is a byproduct of the behavioral mechanism. It is an epiphenomenon. Chronic experiencers need counselling, to convince them that the pain is ineffectual, and therefore not real, at least not in any serious way.

Unfortunately, I get to participate in this second shot at commutative reduction, too. It will go just as well as the first.

 

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Is a Virus Alive?

life, living matter and, as such, matter that shows certain attributes that include responsiveness, growth, metabolism, energy transformation, and reproduction. – Encyclopedia Brittanica

Close enough, and encompassing the generally accepted criteria: responsiveness, reproduction, metabolism and adaptation. My older son asked the question about viruses the other day. I have been looking forward to this question. It means that he is prepared to understand some things about life which are important. It is a tricky question if considered from the wrong viewpoint. A virus displays some of the characteristics which define a living organism. It can respond to stimuli, attaching to the proper cells and injecting its genetic material through the cell membrane when it makes contact. It can replicate. It can adapt to avoid a host immune response. But it does not have the capacity to metabolize. It cannot, in other words, run its own show. It is entirely dependent on its host organism in that respect. Nor is the virus alone on the gray borders of life. Certain families of bacteria lack some essential metabolic processes which would make them autonomous. They must live inside another cell, and depend on their host’s metabolism to survive. Yet, they too can reproduce, adapt, and respond to stimuli in their environment. Because they have a membrane which is active, biologists are prone to give obligate intracellular bacteria, like mycoplasma and Rickettsia, a break. Most biologists are less charitable when it comes to prions. Prions are mis-folded proteins which replicate by somehow inducing their own conformal change in normally folded proteins with which they come in contact. Prions can reproduce, but they cannot metabolize. They cannot adapt much (although they have managed to pass from cows to humans), but they can respond to their environment, albeit in a very limited way. Still, the difference between the prion and the obligate intracellular bacterium would seem to be one of magnitude rather than quality. Differences in their classification reflect a little bit of membrane chauvinism on the part of biologists. The same prejudice is evident in the gray zone at the other end of the complexity scale. By our criteria for life, is a male angler fish alive? The fish can survive for a short period of time independently, but it cannot carry on its own metabolic processes independently for the long-term. It must rely on a female angler fish. It must quickly sniff out a female and attach itself to her, permanently. The male fish spends most of its existence as a tissue of the female angler fish’s body; its brief, free swimming existence is a transitional aberration. Its ability to adapt is extremely limited. Its existence can be mapped on an algorithm only barely more complex than the one which describes a prion’s lifestyle. So what does differentiate the male angler fish from a mycoplasma bacterium, a virus, or even a prion? A few extra membranes make the only difference. Even our own status as living things is at risk if we apply our criteria strictly. We can certainly reproduce, just like the viruses, obligate intracellular bacteria, prions, and angler fish. But it is questionable whether or not we can independently metabolize. We actually rely on hereditary intracellular symbionts for our primary metabolic process. Without these symbionts, our mitochondria, we could live only minutes on the metabolic processes encoded by our own genetic material. So, we can hardly be blamed for fudging our criteria. We certainly want to call ourselves alive. Since it looks and acts alive, we want to call the male angler fish alive. For practical purposes, we also want to call Rickettsia and mycoplasma alive, as well as viruses from time to time. As for the prions, it is often more convenient to view them as sophisticated toxins rather than living things. And that’s the upshot of my son’s question. The issue of whether or not a virus is alive is only confusing if we consider “life” an actual, efficacious thing. But life is just a category. When we look out across the terrible landscape of things, we see phenomena which cluster about each other by dint of their shared heritage. Our account of our cluster is biology, and our criteria for life provide the outline for our biological stories. This is correct viewpoint on the question of life, and what is alive. But this is not the popular viewpoint. The popular viewpoint attempts to preserve life as a thing, as vital essence or emergent property. Unfortunately, the popular viewpoint is not feasible. It leads inexorably back to the original question rephrased, “where is the life in a thing to be found?” In the end, we find that the essence or the emergent property is explained by the operational mechanisms and properties of the thing in question, but it in turn, explains nothing about the thing; it just notes where that particular thing lies on the vast, terrible landscape of things. Despite its glaring inadequacy, the popular viewpoint remains popular because it seems to save us from losing an idea that we don’t feel comfortable losing. But we don’t need to worry, becoming a category doesn’t vitiate life. We have the things which the category marks clustered around us after all, even if it’s only according to our viewpoint. We can’t escape life anymore than we can climb out of our skins. So, the answer to the question? Sure, a virus is alive – as long as you can explain why.

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