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I am blaming bad roads for a broken axle? First of all, with the exception of metal fatigue, an axle does not have the capacity to change in structure and function over time. Unlike a human, it cannot increase its aerobic capacity, change its BMR, energy usage proclivities, insulin sensitivity, cortisol profiles, GH and sex hormone production, bone density, immunologic reactivity, etc. in response to its environment and the chosen interaction with it. The axle in my car cannot make informed choices about diet, exercise, and stress management that will produce concordant changes in both physiology and anatomy. The axle geometry in my mustang will not change to a more optimal one no matter how much I wish it would, short of ripping it out, and putting in a GR-40 kit. But a person's posture can certainly change.
I don't like to give up on patients. And I don't like patients to give up on themselves. Sure a 65 year old with a bad knee and SOB is unlikely to reverse her CHD or DM2, but she can certainly improve her cardiopulmonary function, perhaps to the point that SOB is no longer a problem. Cardiopulmonary rehabilitation is after all one of the most effective tools in improving cardiac function in those with CHD and CHF. And perhaps with improved attention to diet and exercise she will lose enough weight to find that the knee pain is decidedly easier to live with, can help her avoid opiates, and perhaps avoid the long recovery associated with knee replacement. That selfsame attention to diet and exercise will likely improve her A1c effectively and help her stay on monotherapy longer. It can also prevent her from losing toes, going blind, or needing dialysis for the rest of her life.
Sure, she will need medical treatment. Medical management of her cholesterol, fluid status, and A1c will be vital for her. And she may require any of a range of interventions in order to maintain mobility and functionality. But arguing that harnessing the human body's capacity for change in order for her to mitigate the damage to her body and improve her quality of life is just plain ridiculous.
And as a physician researcher, my job is not only to treat, but also to improve understanding of the human body in health and disease and, IMO, first and foremost, to stress primary and secondary prevention. If I can learn how to help my patients and the world at large avoid the debility of disease, it is in everyones' best interest to do so. The 65 year old lady may always have a long list of conditions on her PMH, but if we can educate her on the controllable etiologic factors, perhaps she can help her daughters and grandfathers avoid her fate.
Probably just wasting my time wanting people to actually be healthier rather than relying on a laundry list of meds to do the job for them.
So the biological psychiatrist is now casting doubt on biological psychiatry. That is just wonderful. Maybe you have not read this literature much, but let me make it clear. There are clear changes in brain activity seen in the depressed population on fMRI, SPECT, and PET that are not witnessed in the healthy population. Placebo responders show different patterns of activation than those at baseline, and placebo response is different from treatment. Treatment with medication or with psychotherapy result in patterns of activation similar to those of healthy controls. This has also been shown to be the case for psychodynamic psychotherapies.
There are biological changes associated with a disease, and biological changes associated with treatment discrete from those seen with placebo. These biological changes result in the restoration of an activation pattern of the brain similar to that of healthy controls.
You raise the point of the cyclical nature of MDD, which is funny, as I think that this aspect of MDD is where psychotherapies and behavioral techniques really shine. As we both know from the evidence, this is one of the reasons why antidepressants must be taken for quite some time after symptoms resolve. Otherwise, they will simply relapse within a few months of discontinuing medication. SSRIs result in the normalization of brain function as measured in several different ways, including hippocampal and PFC function as well as factors viewed at the level of the individual neurons involved in serotonergic synapses such as serotonin transporter functioning and receptor regulation. Take away the SSRI, and the patient begins to decline back in to depression, with concordant pathological changes. On the other hand time-limited psychotherapies only last from 8 to 16 weeks, far less than the 2y with antidepressants. But, in long-term followup we see a pattern quite different from the waning effect sizes seen in long-term followup of patients on antidepressants, even in patients who remain on their SSRI. Instead, we see a stable or even increasing effect size long after the therapy is concluded. This has been replicated in many studies, by the way. While what proceeds is inferential, all theorizing ultimately is.
What I can conclude from this well-demonstrated pattern is that while SSRIs may return the depressed patient to a pattern more consistent with healthy brain function, over time, underlying pathologic processes overcome the ability of the SSRI to maintain normal functioning. Contrast this with psychotherapy which also improves brain function profiles in the depressed, which has a long-term maintained, or even improving effect, despite cessation of the active therapy. This implies a direct interference with the underlying pathological process, rather than simply healing the consequences thereof.
Again, this compares favorably with more advanced models of the pathogenesis of diabetes. While an insulin sensitizer alone may decrease A1c for a time, if dietary and exercise factors are not changed, the patient's glucose control will continue to get worse, and over time higher doses and more medication will be needed to maintain adequate glucose control due to continuing worsening in insulin resistance. On the other hand, if early enough in diagnosis, a patient embarks on a brief but high intensity program of instructed evidence-based nutrition and exercise protocols and education, they may completely reverse their insulin resistance, and maintain this effect long after the brief intervention is concluded.
You can raise all sorts of niggling little arguments against such evidence. But ultimately you can with ALL scientific discourse. But the overarching point that is that the neurobiological correlates of disease and treatment are similar whether one looks at psychotherapy or 'biological' treatment. If psychotherapy results in changes to the biology of the brain that correlate to resolution of symptoms, and medications do the same, how exactly can it be argued that medication is 'biological' but psychotherapy is not?
I actually won't argue with much of this. As you and I agree on, based on your earlier remarks, psychodynamic psychotherapy and psychoanalysis lie on a continuum with a common underlying model. Psychodynamic psychotherapies have been manualized, and studies have been done with as rigorous attention to scientific method as has been achieved with CBT.
The truth is, life is messy. Thought is messy. The experience of mental illness is messy. It turns out that in fact, BOLD changes on MRI are not the greatest thing since sliced bread, which has nearly brought many a neuro-imager to his knees with thoughts of seppuku. The biochemical changes seen in the mentally ill turn out to not be as cut and dried as bench researchers had hoped, with many different mechanisms having been elucidated, none present in ALL who suffer from any mental illness. This makes science harder to do and makes conclusions about such issues necessarily a little less certain. But not so uncertain we should throw up our hands and walk away. One of the things that Popper paid little attention to, but something that people from the ancient Hindus to modern physicists have thought about in great detail is the fundamental uncertainty of truth and knowledge. One of the dangers of science is that it is practiced by individuals who are biased. To live and breathe is to hold a bias. Avoiding it is impossible; it can only be acknowledged. One of the dangers of bias is ignoring the uncertainties inherent in the evidence for one's position, while highlighting the uncertainties of the opposite position.
I'm not one to throw the baby out with the bathwater, and I am grateful for my strong education in matters that were classically of high import to scientists, such as the philosophical concerns addressed above. There continues to be a lot of uncertainty in all aspects of brain science, especially where it concerns mental health.
However, I do believe that we can attempt to build more robust theories of mental health and illness by incorporating the broad array of evidence at hand. Which is something that we as a profession have been terrible about.
The problem with this thought is that it doesn't make any sense from an evolutionary perspective. As most of us acknowledge, mental illness can be devastating. Why would evolution select for something that makes it harder for you to think, harder for you to respond, harder to stand up in the face of the life-threatening world of our ancestors? Answer: it wouldn't. And mental illness most often begins to rear its ugly head at precisely the worst time, evolutionarily speaking. Our adolescent and reproductive years. Rates of mental illness are also arguably increasing, as it is hard to fully explain the demographic changes seen in rates of mental illness solely on the basis of improved detection. For a trait to increase rapidly in just a few generations requires a correspondingly large selection pressure in its favor. Now what kind of selective benefit would accrue to the mentally ill that they would have so many more children than others to account for such changes. Depending on what range of realistic assumptions of the model, the rate at which those with genetics that predispose them to mental illness reproduce is anywhere from 1.5 to 8x the time of the general population. And that is being generous when inputting heritability characteristics into the model.
On the other hand, one of the lessons of evolution is that traits and genetics are adaptive in the context in which they evolved and that when placed in a different context may be maladaptive. A dolphin is the most supremely well adapted mammal to a life in the sea. Put it in the desert and it doesn't exactly do well. One of the interesting facets of human evolution is that our gigantic and flexible brains have allowed us to substantially change our ecologies, patterns of development, and interaction with the environment without requiring a concurrent change in basic biology. This coupled to the fact that selection pressures have been severely reduced means that there is not a lot of inherent, structural, and genetic biological change to go along with the huge changes in how we live.
I mean, one need only look at Nariokotome Boy, 1.8 million years ago with a cranial capacity about 40% of ours, to see how precious few changes have been wrought between this hominin whose 'culture' consisted of a slight refinement in the nut-cracking Chimpanzee, and the modern human. It's really quite a profound experience to realize this.
"we are biologically determined to get sick," is one of the silliest ideas on the planet. We are biologically determined to age, and to suffer the slings and arrows of degenerative disease, which mostly (at least in the past) affects us after our reproductive years have passed and is thus evolutionarily neutral. But we are not biologically determined to get sick during the most productive and dynamic years of our lives. This argument, which I hear upsettingly frequently, belies the pathetic nature of evolution education in biomedical sciences.
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You claim life is not pathological, and that neither are the changes in the body associated with it. And yet how many medical disorders are determined in large part by life and the change associated with? CHD, DM2, osteoarthritis and spinal disease, dementia, cancer, HTN, renal disease, osteoporosis, to name a few. The list is long, and it includes some of the most prevalent and debilitating diseases we suffer from. But it somehow does not apply to the brain? The most mutable and exquisitely responsive structure in the human body? That is quite a leap.
I readily admit that it is also still quite a leap from what we know about the brain to what we know about thoughts and experiences. It's a problem for both 'biological' psychiatrists as well as those with a more psychotherapeutic and especially for those with a psychodynamic orientation. But what we do know about the brain is that its function is a result of complex interactions between genes, developmental-environmental interaction, and experience itself. We know that every time a synapse fires, the very structure and function of brain pathways change. We know that brain pathways and cells themselves change in a multitude of ways including changes in resting potentials, number and latency of channels, neurotransmitter production, transporter protein function, and a range of glial changes that we are just now starting to understand. We know that many if not all of these structures and functions are affected to one degree or another in a range of mental illnesses. We know that both medication and psychotherapy can result in normalization, or at least prevention of further pathological changes in structure and function.
But unlike medication, psychotherapy seeks to change the very way the brain functions in and of itself by manipulating its higher levels of function. While much remains to be understood in how it may exert these beneficial effects, strong, if limited, evidence exists for its ability to do so at every level of analysis at which the brain can be studied, from behavior and symptoms, down to biochemicals.
With a better understanding of the link between brain physiology, thought, experience, and psychotherapy will hopefully come a way to limit the depredations of genetic load of psychiatric disease, and prevent the pathological changes that lead to mental illness in the first place.
--Tis a consummation devoutly to be wished--
Calling an idea "the silliest on the planet" before learning what the idea entails is substantially sillier, n'est pas?
Sorry if I can't keep up with your prolific, yet tangential, writings. Must be my age. "Maybe you have not read ... literature much", you said. Thank you, I'll be doing just that.
