Likewise cognitive behavioral therapy and similar work well for many folks. It helps give people tools to change negative behavioral patterns.
There’s fMRI which can objectively show brain activity differences for various mental illnesses.
One psychiatrist could see a patient completely differently from another. You either have Alzheimer's or you don't. Your arm is broken or it isn't. It's measurable.
With mental illness, the line is blurred. I've never seen compelling evidence for fMRI - just circular reasoning. Psychiatrists who buy into this paradigm posit that the disease exists because in these populations of heavily medicated, subjectively diagnosed (heavily traumatized/stressed) individuals, there are similarities between them in the activity of their brain.
Perhaps it's just their disease-first perspective that I take issue with when it comes to fMRI. You could validly look at these populations completely differently without subjective disease terminology and be logically sound with your findings, such as; people tested who experienced more traumatic events in their lifetime and seeing how their brain lit up vs. people who did not experience traumatic events. Or how people respond in institutionalized situations vs. less formal situations, etc.
The person you are responding to shares the same general thinking that I have: medically, there is no disease if there is no measurable physical damage.
As a doctor when you are arguing that somebody has a disease, especially a disease that is thought to be lifelong or perhaps genetic in nature, it's your job to prove that. A check-list of symptoms isn't enough proof. And by going through these lists you are stereotyping your patient. Studying people diagnosed in this way and forming correlations in these heavily stressed, vulnerable populations proves nothing besides perhaps how stressed they are and the different ways that stress is expressed throughout the population.
But when you factor treatment into the mix, physical study of the brain frankly becomes worthless if you are applying it broadly. It could be that fMRI is more or less finding that people on Lexapro or Lithium (whatever the common prescription for an illness is) respond a certain way. Or that individuals experiencing specific types of heightened states (like mania) respond a certain way.
What we are not saying is that there is not suffering, that symptoms don't exist, that symptom groupings (like ADHD) aren't bad or good, it's the disease terminology and intellectual dishonestly of the psychiatric field that we are pointing out.
If somebody took anti-psychotics, especially for a long time, it's known that they affect brain structure and that invalidates any findings that the study has, unless they can account for the changes that the (for example) anti-psychotics produced. Which given our current state of science, and understanding of the brain, is unlikely.
>Initially during the prodrome, a change in brain structure seems to be present in the temporal lobe volume and cingulated. On follow-up in those who have gone onto a psychotic episode, further changes can be seen in the cingulate, temporal lobe, and parahippocampal gyrus.
Structural changes occur before an episode has even occurred.
Upon a very, very brief read it still seems difficult for them (in my opinion) to find that schizophrenia is primarily genetic in nature when there still could be potential causative agents that only siblings share (the same house, the same food and water, the same household/generational chemical/drug use/exposure, etc.) which may yet explain the changes/differences. I will take a closer look when I have the time and look at the wealth of references they included (they do have some pretty large studies referenced that support their findings). Thanks again.
I just want to say that while I may seemingly appear to be particularly hostile to the physical causative angle or the genetic (or predictive) angle of mental illness, I just want to clarify that this is mostly because of the fears I have about the current/near-future clinical/societal implications of this being established, in my opinion, prematurely.
There's unarguably a lot of good that research can do in this area, however, I just hope that more understanding in these areas are reflected clinically by a massive diversity of treatments. Especially, laser-focused treatments that cause minimal side effects.
I don't think there's any arguing from me that if we were able to stop the progression of schizophrenia before first-episode psychosis (especially without using anti-psychotics long-term or at all) that it wouldn't be a good thing.
Or as other commenters pointed out, to stop these people who share these markers from doing things that might worsen/manifest their illness, like cannabis. Or researchers finding out how the endocannabinoid system is involved in the illness, including potential therapies (like tackling the systemic inflammation that is common in serious mental illness).
It's just a slippery slope if we go about this in the wrong way. Like forced treatment. Or applying treatments to other differences that may not cause distress to the individuals or inhibit their functioning or participation in society (like forcibly treating high functioning individuals who are on the autism spectrum).
Or incorrectly diagnosing schizophrenia/psychosis in one person and inappropriately treating them, when in reality there were two or three distinct diseases causing a similar illness or set of symptoms. Who knows, there is a distinct lack of knowing still in this field. I just know that the profit-motive needs to disappear before true progress and medicine can happen.