Creativity
Making our way into the world…
Creation
Patterns coalesce.
Imagination runs free.
Brilliant or mad?
The boundary between genius, creativity, brilliance, on one side, and madness on the other, is thin and porous, with one leaking into the other. Aristotle is quoted as saying, “no great genius has existed without a strain of madness.”
Vincent van Gogh was a prolific artist whose works today command hundreds of millions of dollars at auction. He is also widely acknowledged to have been mad, cutting off his own ear during a dispute with another artist. John Nash was a brilliantly creative Nobel-prize-winning mathematician, a prodigy who suffered hallucinations and was incapacitated by schizophrenia. Nikola Tesla single-handedly invented the alternating current (AC) electrical distribution system we use around the world today, displacing the DC system and thus earning the lifetime enmity of the most powerful inventor of the time, Thomas Edison. Tesla’s inventive genius was unmatched, but his career was cut short as he descended into mental illness. Abraham Lincoln was a self-taught political genius who clawed his way out of the backwoods of Kentucky to become president and the Great Emancipator. Lincoln also suffered severe bouts of depression and is widely thought to have penned the poem The Suicide’s Soliloquy, which included the lines:
Hell! What is hell to one like me
Who pleasures never knew;
By friends consigned to misery,
By hope deserted too?
This is the same president who penned the immortal words of the Gettysburg Address, which closed with lines that ring on even today:
… that government of the people, by the people, for the people, shall not perish from the earth.
Some of history’s greatest geniuses clearly suffered mental anguish. Ludwig von Beethoven. Winston Churchill. Charles Darwin. Charles Dickens. Kurt Godel. Ernest Hemingway. Isaac Newton. Michelangelo. Robert Schumann. Leo Tolstoy. Virginia Woolf…
But a list of great sufferers doesn’t prove anything.
A recent Swedish study examined 300,000 people with severe mental illnesses, compared to family members without a diagnosis and unrelated controls. The authors of this study concluded that people with schizophrenia and bipolar disorders (and their closest relatives without known conditions) were more likely to work in creative occupations such as the arts and sciences compared to controls. This association was not found in people with unipolar depression or their relatives.
This association also disappeared in relatives more distantly related to those suffering from schizophrenia and bipolar disorder. The researchers concluded that there was a genetic link between risk for mental illness and creative occupation.
The authors of the Swedish study also noted an important evolutionary point about the preservation of psychiatric disorders throughout human evolution:
“…alleles to mental disorders in patients or relatives also harbour adaptive advantages that increase fitness.”
In other words, gene variants that may lead to some mental disorders could be preserved evolutionarily because they also provide advantages which outweigh the disadvantages. The authors quote studies which suggest that bipolar disorder may have been an adaptation for long winters, and that schizophrenia may have been a consequence of evolving language. The individual and social benefits of creativity are one we might throw into the ring, the evolutionarily advantageous benefits to the suffering of psychosis.
But clearly, there is a wide range in the level of creativity and the degree of mental illness. Does an off-the-charts genius level of creativity carry with it larger risks of mental incapacity? Is there a madness dial where you can tone down the voices in the head so one can be sufficiently functional and creative, get out of bed, find the coffee maker, and write another chapter?
Destruction
Gene regulation.
Balanced between good and bad.
Artist or patient?
Studies like the Swedish one examining large numbers of people are powerful in their ability to tease out hidden associations. But associations are inherently limited because they are unproven links, in our case, links between mental illness and creativity. To prove a link, we need to uncover mechanisms, demonstrate cause and effect, digging deep into the genetics and biochemistry of creativity and madness.
One possible step towards that mechanistic understanding is a study that claimed to find a specific genetic polymorphism, a variation, in a gene called NRG1, which is associated with both high psychosis risk, as well as high creative achievement. The key word there again is “associated.” This is still an association study, even though it is a genetic association.
A gene called neuregulin 1 (NRG1) has been under investigation for increased risk of psychosis. This particular variant of NRG1 has a change in what is called the promoter region, the switch part of a gene that controls whether that gene is on or off and how much of the protein NRG1 to make.
Many view the NRG1 gene as a likely candidate for susceptibility to schizophrenia. NRG1 is located in a part of a chromosome (numbered 8p), which genome-wide association studies have linked to schizophrenia. Furthermore, NRG1 has been linked to schizophrenia in many population studies around the world. A major challenge, however, is the failure to find any mutation in NRG1 linked to the disease. This lack of mutations in NRG1 has led some researchers to propose that the variation is a non-coding change (one that does not affect the amino acid sequence of the NRG1 protein). Rather the change affects how much or how little NRG1 is produced.
Digging deeper into the genetic associations of NRG1 with schizophrenia, other researchers suggested specific transcription factors, protein switches that bind to the promoter region of genes. These researchers linked three transcription factors to the modified region of the NRG1 promoter linked to the disease.
We cannot emphasize enough that these are all still association studies. We are all pointing at a suspect who has been found at the crime scene, but no one has proven beyond a reasonable doubt that the suspect committed the crime. We have not yet proven that variants of NRG1 cause schizophrenia.
And what is missing are experiments showing that variations in NRG1 promoter leads to variations in NRG1 protein levels, and these level changes cause schizophrenia or health depending on how you turn the dial.
Kali Goddess of Creation and Destruction
Evolution makes
species by destroying those
who can’t procreate
Cells control proteins
by balancing creation
with their destruction
Genes that elevate
the brilliance of a few
destroy yet others
To review where we are today… population genetics and demographic studies show a linkage between creativity and some mental illnesses such as schizophrenia and bipolar disorder.
This is bolstered by data linking a specific chromosomal region and a gene called NRG1 located within that region to both psychosis and creativity.
However, researchers have not found any schizophrenia-associated mutations in the NRG1 protein encoded by the NRG1 gene.
Others, have found changes in the promoter region of NRG1, to be associated with schizophrenia. These promoter changes, in turn, are associated with transcription factors that turn NRG1 on or off.
The transcription factors are called serum response factor, myelin transcription factor-1, and High Mobility Group Box Protein-1.
Varying levels of NRG1 protein are hypothesized to lead to psychosis or health.
The level of NRG1 is, in turn, set by the creation and destruction of the NRG1 mRNA and/or proteins. Kali turns at the heart of our cells, dictating health or death.
Perhaps, we know some, finding out more each day and there is much more that remains unknown — and the scientific quest to find the “genes” of creativity continues…
For thousands of years we’ve sensed that creativity and madness are two sides of the same coin (Aristotle was probably not the first to voice his point). Narrowing the biology of creativity and madness to a single gene, NRG1, and more importantly to the promoter controlling that gene, we seem to confirm our ancient observations. And if creativity is indeed an unstable gift, balanced on the verge of tumbling into madness, what are we doing by programming machines to be creative? Would we recognize when these machines run themselves off the rails? Most of these creative AIs are self-programmed by Generative Adversarial Networks (GANs), meaning AI scientists have no idea how these programs do what they do. By creating these GANs and creative AIs, are we building the seeds of madness into our machines? Can we trust machines like these?
One blessing is that we can design tests to challenge the stability of these AIs, and confirm the rates at which they produce unacceptable results that suggest a “psychotic” process. Just like we want our self-driving AI cars to crash at levels far below human drivers, we want creative AIs to also “crash” much less frequently than human creatives.
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