Once again, the answer is not as obvious as it seems.
It is true that if no known general medical condition can be determined to be the cause of the symptoms, the person can be diagnosed with a “mental” illness such as “schizophrenia” or one of the related illnesses such as “schizoaffective”.
Let’s say the person took one toke of marijuana too many. Or let’s say we even know for a fact that the person seemed fine until the loss of a loved one . Or they just got increasingly psychotic and delusional. Let's say there doesn’t appear to be anything else wrong except that now they went “nuts”… maybe even catatonic. Let’s say they “responded” to antipsychotic medication and got “all better” (usually there is still some degree of impairment because of the physical problems to be discussed).
Let’s say, the illness really fits what is called “schizophrenia”.
That still does not mean that the illness is not a real physical illness with real physical suffering and real physical damage.  That physical damage may have been triggered by an interaction of genes with the environmental insult of cannabis or the psychic stress of the loss of a loved one, but the resulting damage is still physical.
The physical damage wrought by the disease is what is being studied with expensive machines and millions upon millions of dollars being poured into scientific and medical research. By understanding that (physical) disease process, it is hoped we can provide better treatments. If it were merely “mental”, we’d just be putting them all into therapy “to snap them out of that catatonia” or “just stop those hallucinations”. The damage can be seen on MRI and through chemistry. Not only is there damage to the brain (loss of brain tissue), but there can be widespread oxidative stress, damage to mitochondria, increased incidence of diabetes, more hormonal dysfunctions, and more!
It is no different than diabetes, Alzheimer’s, or multiple sclerosis. In fact, some people with schizophrenia may have damage to the myelin sheaths surrounding nerves in the brain (myelin sheaths are involved in other medical illnesses such as multiple sclerosis (MS). Note that at one time, MS was also considered to be “mental”).
And if it is physical, it isn’t really “mental” at all. The person may seem to have “mental problems” such as not being able to handle stress, or having anxiety, but many illnesses we do not call “mental” does that as well, such as Addison’s, MS, Cushing’s, low thyroid, and other autoimmune, adrenal and pituitary problems.
Once upon a time, medical doctors knew schizophrenia was a real physical illness. The era of “Freudian Psychology” in the absence of modern research techniques, swung the pendulum to the belief that even these severe disorders affecting the brain were “psychological” and with correcting the faulty thinking through psychotherapy (or behavior modification for psychotic “behavior”), they would be “cured”. This was actually not Freud’s fault. As far as I have read, Freud never worked with people with these severe illnesses affecting the brain (i.e. “schizophrenia”). People just tended to apply his theories to everyone.
When they do something that seems bizarre or even outrageous, the person they were, with the normal unaffected brain they had before the illness damaged the brain, would have been mortified to know what they are now doing. It is no different than that prudish reserved former minister who gets a dementia and is found wandering the street half naked. It is not that person’s fault. The BRAIN is affected. That is the case with schizophrenia, as well. The BRAIN is affected.
The illness is not just some psychological or emotional (i.e. “mental”) problem people have. This is a complex physical illness that deserves the proper medical treatments that people with any other “physical” illnesses have.
- There may be a gene-cannabinoid link. Cannabinoids and psychosis. See also: Brain Scans Reveal How Gene May Boost Schizophrenia Risk and Interpreting the association between cannabis use and increased risk for schizophrenia.
- Acute stress in adulthood seems to exacerbate the problem in early stages of schizophrenia and interacts with underlying biology but may not “cause” it by itself. Life events can trigger depressive exacerbation in the early course of schizophrenia. There is a larger connection to traumas and stressors in childhood to the development of many medical problems (including schizophrenia) later in life such as diabetes, lupus, arthritis.
- There are hundreds of research articles each year on the physical aspects of “schizophrenia” including cell death, nerve changes, mitochondrial dysfunctions, etc. Here is just a brief sampling:
a. Apoptotic mechanisms in the pathophysiology of schizophrenia.
b. Emerging principles of altered neural circuitry in schizophrenia.
c. Mitochondria, synaptic plasticity, and schizophrenia.
d. Disrupted in Schizophrenia 1 (DISC1) is a multicompartmentalized protein that predominantly localizes to mitochondria.
e. The ultrastructure of lymphocytes in schizophrenia.
f. Selective deficits in prefrontal cortical GABAergic neurons in schizophrenia defined by the presence of calcium-binding proteins..Biological Psychiatry
- Again here are just a few references:
a. Variations in myelin and oligodendrocyte-related gene expression across multiple brain regions in schizophrenia: a gene ontology study.
b. White matter changes in schizophrenia: evidence for myelin-related dysfunction.
c. Neuron-specific enclose and myelin basic protein in cerebrospinal fluid of patients with first episode schizophrenia.
d. Targeting synapses and myelin in the prevention of schizophrenia.