From the medical point of view, the biocognitive model of mind has great predictive value. It says, for example, that the mind will be able to influence the body's function without the individual actually knowing how he does it. Information from the body influences the mind silently and at high speed, and the mind does the same in reverse. That is, it provides a basis for a model of psychosomatic medicine, a field that allopathic medicine has never been able to grasp. The reason for this particular failure of the reductionist model is that it recognizes only one-way action, from body to mind. The new dualist model says that there is two-way interaction between mind and body. This has the immediate consequence of suggesting that, under certain conditions, mind and body can set up feedback loops with unpredictable effects. In medicine, of course, we are interested in negative feedback loops, such as the maladaptive states that represent psychosomatic illness.
If we take a very simple example, skin rashes always seem to be worse when people are anxious. The dualist model says that the rash worries the patient and the worry makes him sweat; when the sweat enters tiny breaks in the inflamed skin, it causes itching, which the person then scratches and thus makes the rash worse. Similarly, a person who fears heart disease will worry over every tiny blip in his pulse rate; but anxiety causes many blips in the pulse, which convinces the patient that there is something seriously wrong with his heart. The clearest example, of course, is psychogenic impotence in men. A man worries about his sexual performance, but anxiety inhibits male sexual performance and so his problem gets worse, which convinces him there is something seriously wrong and makes him worry more.
Management of anxiety in this model relies on rectifying the patient's destructive belief system. That is, we would use one or other form of psychotherapy to assist the patient in abandoning the old, damaging belief system and replacing it with a set of beliefs consistent with the facts of the real world. Simple forms of this psychotherapy would be essentially educational, such as, “You needn't worry about catching an infection. Your body has plenty of defenses.” The more far-reaching forms of therapy would involve taking the patient back to the times he acquired his maladaptive beliefs and reorienting his entire mental set on the world and on himself.
Within the field of psychiatry, the biocognitive model explains anxiety states remarkably well without invoking primary “chemical imbalances of the brain.” The “cognitive” part says that an anxious person is just a person who responds to neutral events in the environment as though they were threats. That is, the patient misclassifies events as dangerous when, objectively, they are not. The patient then experiences the appropriate emotion (anxiety) too often and too intensely. Note, however, that the model predicts the patient's brain is normal: he is simply mistaken in his beliefs. If there are any “chemical imbalances” in the patient's brain, they are secondary to the beliefs and therefore are not primary pathology. Similarly, a panic state is just a self-reinforcing state of high agitation, where the person worries about the physical effects of anxiety (eg, shortness of breath, palpitations, gastric upset). However, worrying about the somatic effects of anxiety breeds more anxiety, so the process quickly becomes self-sustaining. When it settles, the patient is more afraid than ever of the first stirrings of anxiety, and a new panic becomes more likely because he has already had one. It is no coincidence that panic states often start when the individual is recovering from a viral or other debilitating illness.
When we turn to depression, the modular approach in the biocognitive model has immediate explanatory value. We can take the grief response as the archetype of the depressive reaction. The model says that the person realizes that he has experienced a substantial loss. Signals are then sent to those emotional centers, which subserve the sense of enjoyment and pleasure, effectively paralyzing them. We assume that this involves activation of the genome to produce chemicals that block neural transmission or even stimulate the outgrowth of inhibitory synapses.
22 They no longer respond to normal input with activity that the individual experiences as “fun” and that is accompanied by stereotyped behavior such as laughing and clapping the hands. Life appears flat and colorless, and this persists for months until, slowly, the period of emotional paralysis wears off. Note that the neuronal inhibition induces a psychic paralysis. This conceptualization of depression, as a normal response to an abnormal event, even indicates where drugs and ECT have their effect. We would assume that antidepressants and ECT function at the synaptic level to overcome the temporary biological blockade before it would normally wear off. This would also explain why people relapse if the antidepressant is stopped too early. With drugs or ECT, the original neuronal blockade has not been reversed—only overcome functionally.
The fraught relationship between depression and anxiety, so often dismissed as “comorbidity,” assumes a different light when seen from the point of view of a model of dualist interaction. Most surveys show a very high coincidence of anxiety and depression, far higher than chance alone would predict. Cases of depression as a reaction to a pure loss show very little anxiety but these types of depression cases are a minority. Using the model of negative feedback, we propose only that chronic anxiety seriously affects the quality of life, to the extent of making the patient feel hopeless about his prospects. He experiences a major loss of hope—the state we call depression. That is, chronic anxiety causes recurrent depression, as my series show.
12 For the treating psychiatrist, the significance is that unless the anxiety state is treated in its own right, it will flare up as soon as the (sedating) antidepressants are stopped, meaning the patient is at risk of a further bout of depression. It is for this reason that antidepressants are now prescribed long-term and often in conjunction with other sedating drugs called mood stabilizers. They function to stabilize the mood because they stabilize the anxiety which destabilizes the mood in the first place.
Elsewhere, I have outlined a cognitive model for psychosis
11 that predicts that the familiar split of the functional psychoses into affective and schizophrenic is artificial. In briefest terms, it says that psychosis is the manifestation of a failing mind—not of a failing brain—and minds can “fail” for a variety of reasons. These reasons include intense and protracted psychological distress, drugs and other intoxications, metabolic problems, slowly progressive brain disease, and the confusing effects that mild, diffuse brain damage may have on the individual's contact with the world. It is for this reason that orthodox psychiatry keeps finding structural, biochemical, and now genetic faults in a proportion of people with psychotic disorders.
The history of psychiatry is thronged with people who have “discovered the cause of schizophrenia.” The biocognitive model says that as the technology advances, more and different lesions will be found, but not one of them will ever be causative of the condition. It also says that cognitive therapy of the psychotic states is not only feasible but also almost certainly essential in managing these conditions. Perhaps this is the explanation for the endlessly mystifying fact that schizophrenia in developing countries is not so malign as in the West.