Folie en masse! It’s so tempting to drink the Kool-AidCurrent Psychiatry
By Henry A. Nasrallah, MD
Current Psychiatry and its Editor revalidate a statement made by Dr. Nancy Andreasen in 1994 in an editorial written for the Journal of the American Psychiatric Association she said:
“The Ahistorical Fallacy rests on three faulty assumptions. The first assumption is that ‘proposition X’ must be true because it is what the ‘experts’ are teaching. The second assumption is that ‘proposition X’ must be true because it is the most recent one to be put forth. The third assumption, which buttresses the first two, is that ‘if information increases, knowledge increases as well.”
And this is what Dr. Nasrallah thinks about the “blind beliefs”:
Psychiatrists occasionally encounter a case of folie à deux, where 2 persons share the same false belief. Paradoxically, it is more common for a large number of people to share a false belief (folie en masse) and uphold it as fact because the idea appears enticingly valid as an “explanation” for a problem or event.
“Conspiracy theories” abound in our society and yet conspiracy theory advocates would express shock and disdain at the infamous event when 918 followers of Jim Jones drank cyanide-laced Kool-Aid because they believed their leader’s irrational ideas. Apart from recognizable cults—some of whom claim to have their own “solutions” for mental illness—many ordinary people uphold beliefs that are not supported by evidence but widely “accepted” as true:
Persons with psychosis are dangerous.
This incorrect belief was prevalent before the tragic events at Virginia Tech and Tucson, AZ (remember the “Son of Sam” in New York?) and was reinforced by them. Clinicians know that, similar to the general population, only a small proportion of persons suffering from a psychotic illness exhibit violent behavior. In fact, their illness renders them more likely to be victims than perpetrators of crime.
Atypical antipsychotics are associated with high weight gain, but older neuroleptics are not.
Many psychiatrists uphold this clinical mantra and believe that older antipsychotics, such as haloperidol, which cause a lot of movement disorders, are associated with minimal weight gain. Most also believe that some atypicals are weight-neutral compared with other atypicals. The evidence from the European First Episode Schizophrenia Trial (EUFEST) debunked both beliefs by finding substantial weight gain with all antipsychotic drugs, old or new, after 1 year of treatment with haloperidol and several atypicals (Table)1. Neither old antipsychotics, such as haloperidol, nor metabolically “benign” atypicals, such as ziprasidone, are exceptions. Yet this belief likely will persist.
Source: Reference 1
The U. S. obesity epidemic is caused by too much fast food and too little exercise. This widely accepted explanation sounds like a no-brainer. However, by taking a “big-picture” view, a recent study2 pointed to completely different reasons for rising obesity in the United States. Researchers found that other species such as rats and mice (rarely seen waiting in line at McDonald’s) experienced dramatic per-decade increases in obesity rates over the past 50 years, including 38% in pet cats, 34% in chimpanzees in research labs, 21% in alley rats, and 12% in government lab mice. Only pet dogs escaped the escalating obesity rates with 3% per decade. Alternate explanations for rising obesity include less sleep, which increases ghrelin (an appetite-stimulating hormone) and decreases leptin (a satiety hormone); proliferation of fat cells from chemicals such as bisphenol A; central heating (less burning of calories) and air conditioning (prevents the appetite-suppressing heat of summer); infections such as adenoviruses that can cause obesity in animals; and changes in gut bacteria, some of which increase caloric extraction from food.
Many false beliefs have been adopted by a large proportion of the general population. This tendency for folie en masse is consistent with studies that show pre-psychotic thinking is found in more than half of the general population, suggesting a continuum between psychosis proneness and clinical psychosis.3 This raises the question: could psychosis proneness mean that the brain can produce its own “endogenous” Kool-Aid?
Kahn RS, Fleischhacker WW, Boter H, et al and the EUFEST study group. Effectiveness of antipsychotic drugs in first-episode schizophrenia and schizophreniform disorder: an open randomised clinical trial. Lancet. 2008;371(9618):1085–1097.
Klimentidis YC, Beasley TM, Lin HY, et al Canaries in the coal mine: a cross-species analysis of the plurality of obesity epidemics. Proc Biol Sci. 2010 [Epub ahead of print].
Van Os J, Linscott RJ, Myin-Germeys I, et al A systematic review and meta-analysis of the psychosis continuum: evidence for a psychosis proneness-persistence-impairment model of psychotic disorder. Psychol Med. 2009;39(2):179–195.