We should not overlook the fact that schizophrenia is really schizophrenias (plural). For example pellagra, still around in many parts of the world, may be [mislabeled as schizophrenia]. Similarly, cerebral allergic reactions to gluten (gluteomorphin) can give rise to clinical features that would be [indistinguishable from schizophrenia], and therefore would be [overlooked by most psychiatrists].
Hoffer himself sometimes moved away from the adrenochrome hypothesis. For example, he advised us to think of alternate treatments (i.e., hypotheses) if a patient had not responded to therapeutic doses of niacin. Hoffer considered hypothyroidism as a possible cause of schizophrenia. He even quoted a study by Danziger that showed recoveries in 80 schizophrenic patients that were administered natural desiccated thyroid for at least 100 days, and who were ill for six months or less.
Foster, Pataracchia, Campbell McBride, and others have summarized the alternate causes or hypotheses of schizophrenia, such as subclinical hypothyroidism, cerebral allergy to gluten, sugar and petro chemical inhalants[HUFFING/VAPING?], heavy metal toxicity, and candida/gut dysbiosis. In any individual case, any combination of causes might be implicated in the genesis of the schizophrenia syndrome.
Although, at least to my knowledge, adrenochrome has not been measured and compared between schizophrenic, nonschizophrenic and normal control groups of population, we can draw conclusions in favor of niacin and hence, indirectly for the adrenochrome hypothesis, from Hoffer’s studies and reports that spanned many decades. Outside of Hoffer, there have been publications giving indirect credence to the adrenochrome hypothesis. For example, Wittenborn published data demonstrating that acute-onset patients (ill for six months or less) were having intact inter-personal relations as a result of niacin treatment.
Hoffer’s writings also stressed the value of psychosocial factors when he talked of food, shelter, and respect as critically valuable factors in recovery without psychiatric drugs. In the case of chronic schizophrenic patients, who are likely to develop negative symptoms, much like the well known symptoms of “institutionalization or hospitalization syndrome,” the useful hypothesis may be something other than the adrenochrome hypothesis. There is even evidence of gluten sensitivity in chronic schizophrenic patients. They may have become chronic because the treating physician didn’t consider gluten as a hypothesis of schizophrenia. A 2009 publication described a lifelong schizophrenic patient that recovered following a gluten-free, low-carbohydrate ketogenic diet.