Sometimes it’s not genetic: how Emotional Distress causes psychosis, and not the other way around
The main reason to talk about emotional distress instead of a disease based approach is that it’s more accurate. The well shared theory is that genetic predisposition causes psychosis which causes emotional distress. However, when you look at the details, you’ll find that instead it’s the other way around. Emotional distress causes psychosis which causes genetic change. Many times the root cause is not genetic at all.
Genetic research leads to evidence that emotional distress causes psychosis
The claim that’s been made for many years that “mental illness is genetic.” This is the idea that people experience severe emotional distress because of some kind of weakness or predisposition in their genes. Instead it turns out that emotional distress is a normal human reaction to a really lousy life situation. People who suffer intensely mentally may be more sensitive or perceptive of their situation, as Ken Rosenthal shows in the excellent documentary called Crooked Beauty. He tells how emotional distress causes psychosis and many other symptoms on a complete continuum with “normal” behavior. As Paula Caplan says about PTSD, “Many veterans are being called sick when in fact they are having understandable, normal human reactions to war. War is horrible, and of course people have emotional distress afterwards. Why should not feeling anything be called a “normal” reaction?”
Over 25% of the human genome has been linked to mental illness at one point or another, but very few of these studies can ever be replicated. According to Tim Crow of Brown University, what people say seven times does not neccessarily make it true: “A chorus of reviews come out all the time with titles including ‘The discovery of susceptibility genes for mental disorders’, ‘Genes for schizophrenia ?’, ‘The molecular genetics of schizophrenia’, ‘Schizophrenia – genes at last ?’ This blog borrows heavily from his analysis of those claims to show that emotional distress causes psychosis.
The futile $10 billion search for a “mental illness gene”
The classical approach to find a “mental illness gene” is to use linkage to detect the general region within which a disease-causing gene is suspected. Then a different kind of study called association can locate a particular gene with greater precision, and thus to lead to its identifcation. The reality is that in spite of a plethora of well-hyped findings no linkage claim has proven robust. In each case an apparent finding in a modest-sized population of families that was then used to ‘identify’ a candidate gene has not been found linked in more systematic and larger studies.
Thus the advent of genome scans (unbiased surveys with markers across the whole genome) has not strengthened any of the claims for a genetic cause for emotional distress. The bigger the studies get, the less confirmation there is. Two meta- analyses of the genome scans of schizophrenia and bipolar disorder revealed no strong findings and failed to agree on places in the genome that might even be of interest.
The three largest genome scans, with over 300 sibling pairs, still show little agreement between the studies. There’s also no consistent support for any candidate named as the “mental illness” gene (Crow, 2007). The large genome scans that have recently come out (Sanders et al. 2008) have refuted nearly all of the previous papers claiming a genetic linkage, even though 57 of these papers have been cited over 200 times. The Sanders study looked at a huge list of candidate genes in over 1870 patients and 2002 screened controls and was by the far the biggest of its kind. No evidence of an association at any of the sites was found.
Crow talks about the World Congress of Psychiatric Genetics held in New York in October 2007,
“The discussion was somber. In the morning Francis Collins, Head of the Human Genome Project, had predicted sure future progress with these technical advances. In the afternoon it was seen that just such a strategy had failed to yield decisive findings showing the location of a gene predisposing to psychosis, still less are they in agreement concerning the identity of such a gene.”
Ionnnidis et al. pointed out in Nature Genetics 2009 that lack of reproducibility is an innate characteristic of the majority of microarray-based gene expression profiles. There are several theories about why a “mental illess gene” can’t be found. One is that lots of people might have different genes, despite the fact that psychosis tends to show up the same way at the same age with the same structural brain changes worldwide. Another theory is that maybe there are tons of different “mental illness genes” that each have a very small effect. However, if the effect is that small, maybe it’s not really the cause, anyway. The third theory is that we just aren’t doing big enough association studies yet, even though the bigger studies get, the less evidence we find. This “magical thinking” is pushing funding decisions at places like NIMH who aren’t willing to admit that emotional distress causes psychosis. A great question is why are the thought leaders in academic mental health still talking about evidence based medicine but then working from this disproved genetic narrative?
How emotional distress causes psychosis by modifying gene expression
Crow’s article in Psychological Medicine says that if we don’t have a “mental illness gene,” then how does mental illness happen? He points out that DNA can be changed in a grown person. This is done by three different processes, called methylation, acetylation or phosphorylation of the histones. Histones are bodies that the DNA wraps around so that the 5 feet of DNA in each cell can fit inside. Histones have a big role in gene regulation. In genetics, it turns out that the genes a person has are not nearly so important as figuring out which ones get turned on and off. It also turns out that one gene get removed, altered or turned on, other genes have other effects, so the $10 billion search for a single “mental illness gene” has been completely futile.
Phillip Seeman is a geneticist who has worked his whole career looking at the genetic basis for schizophrenia. He is a person who might, in a slightly different history, have won the Nobel Prize for finding that all psychosis comes from the same source: supersensitivity of the D2 subtype of the dopamine receptors. After a very long and prolific career in this field, Phillip Seeman’s current publication in Future Medicine shows that emotional distress CAUSES psychosis which CAUSES genetic changes.
He says that people’s nervous systems can be exposed to risk through genes, toxins, chemicals, infective agents, lack of oxygen, trauma, or social isolation. This causes the dopamine receptor to move to a state where it’s more sensitive to dopamine. This is a general neural mechanism that helps the nerve cells adpat, repair, and regenerate. It helps to protect the brain from further injury. However, people experience this process as overstimulation. The ways that people psychologically adapt to the overstimulation are the signs and symptoms that have been identified with schizophrenia and other psychoses.
Video showing what I feel like when emotional distress causes psychosis
The sequence of events when emotional distress causes psychosis
To explain how emotional distress CAUSES psychosis, we can look at this cascade that is explained in Phillip’s Seeman Future Medicine Paper. This in an integrated brain and behavior process that provides a much better theory than a single gene weakness to describe how emotional distress causes psychosis, mania, depression, or inability to pay attention.
- brain injury (This could be sexual abuse or other trauma, lack of friends, job stress, drug abuse, toxins, lack of sleep, poor nutrition, or any of the other 30 causes shown for psychosis.)
- adjustment of the nerve cells (This is where the dopamine receptors convert to a high affinity state which has been shown to be common to ALL forms of psychosis. More dopamine receptors also form in a given part of the brain increasing the density of receptors for a double whammy.)
- increased neurotransmission (More affinity and density of the dopamine receptors)
- people’s awareness of being overstimulated (Ken Braiterman is writing a blog now about practical solutions for this awareness)
- psychological adaptation (Symtoms arise from attempts to deal with the stimulus overload.)
- symptom production (Thoughts, self-talk, waking dreams, or vivid recollections are seen as coming from outside oneself and labeled voices or hallucinations. Attempts to withdrawal from social roles, relationships, and expectations are labeled negative symptoms or “avolition”. People who try to shut out the world are told they have a lack of interest, “anhedonia”.)
How Wellness Wordworks provides solutions to emotional distress:
Sometimes it’s not genetic. Sometimes it’s trauma, sometimes a poor job fit, sometimes people are putting too much pressure on themselves to be ambitious, sometimes its drug use, sometimes it’s bullying or oppression in society. This is addressing step 1 in the cascade of events above rather than step 6. This is one of the reasons our program is highly evidence based, why we plan to have much higher recovery outcomes, and why our costs are so much lower. Our job is to help people find complete mental health recovery where they no longer need any kind of medical treatment at all for emotional distress.