Behavioural Geneticist Robert Plomin: ‘There Are No Disorders, There Are Just Quantitative Dimensions’ (Extended)

Behavioural Geneticist Robert Plomin recently spoke with author Sam Harris on the Making Sense podcast (Episode 211 – The Nature of Human Nature). They covered a variety of topics related to the field of behavioural genetics with reference to Plomin’s latest book, Blueprint: How DNA Makes Us Who We Are (see Jay Joseph’s Mad in America article, for an in-depth review).

Given my criticisms of behavioural genetics and its use in attempting to demonstrate the existence of discrete psychiatric ‘disorders’, it was a pleasant surprise to hear Plomin state the following during his conversation with Harris:

I really believe in psychiatry and psychology these diagnoses have held us back, tremendously. And all of the DNA studies—these genome-wide association studies—are case control studies. So, the whole game is to find these people who meet these—what I think are arbitrary diagnostic criteria—and you call them cases, like schizophrenics. And everybody else is a control. And that’s really held us back because it’s just simply not true. . . . I’m basically saying, there are no disorders, there are just quantitative dimensions. And one implication of that, then, is if there’s no disorder, there’s nothing to cure. It’s not like you’re cured, yes or no. It’s all quantitative. It’s a matter of more or less. We’re alleviating symptoms rather than curing a disorder.

It is encouraging to hear leading scientists such as Plomin acknowledge that psychiatric diagnoses are fundamentally arbitrary and that the idea of a ‘cure’ does not make sense with regards to psychological issues.

That said, throughout his discussion with Harris, Plomin repeatedly refers to ‘schizophrenia’, as if it were a discrete disease. Perhaps Plomin recognises ‘schizophrenia’ does not exist and is simply using it as a shorthand for the behaviours and experiences that the label purports to represent. Unfortunately, reading Plomin’s book, Blueprint, did not clear up the confusion; if anything, his views on the matter became even less clear.

“Mental disorders do not exist . . . but causes of mental disorders do”

In chapter 5 of Blueprint, Plomin acknowledges that ‘there are no genes ‘for’ any psychological disorder.’¹ And, mirroring what he said to Sam Harris, he writes that ‘there are no disorders – they are just the extremes of quantitative dimensions.’² However, Plomin also claims that ‘we all have many of the DNA differences that are related to disorders.’³ So, to sum up: There are no psychiatric ‘disorders’, and there are no genes ‘for’ disorders, but we all have genes related to disorders—disorders that do not exist. This is getting confusing.

Later in the same chapter, Plomin again implies a belief in the existence of discrete disorders by stating: ‘common disorders, including all psychological disorders, are not caused by a single gene.’⁴

Regardless of how many genes may be involved, how can one talk about causes of disorders after claiming they do not exist?

But because the genetic risk is continuous, it makes no sense to try to reach a decision about whether someone ‘has’ the disorder or not. There is no disorder – just the extremes of quantitative dimensions.⁵

If it makes no sense to decide whether or not someone has a disorder, how can Plomin claim that certain DNA differences put people at risk for a given disorder? At best, one could make the case that specific genes correlate with types of experiences such as hearing voices, paranoid thoughts, depressed feelings, etc. But even then, are the genes that lead a divorcee to feel depressed the same as those that cause a child of neglect to feel depressed? If one person claims to hear the voice of God and another person claims to hear an abusive parent’s voice inside her head, are the same genes involved?

Since diagnoses like ‘depression’ and ‘schizophrenia’ are just a mishmash of behaviours and experiences that are by no means shared by all individuals diagnosed as such, and since current behavioural genetic research is so hopelessly confounded—in-part, due to the fact that the criteria used to diagnose people are, as Plomin acknowledged, arbitrary—it is difficult to determine the accuracy of the gene ‘discoveries’ touted in Blueprint (or take seriously the idea that these collections of genes can be used to predict future mental states).

In the conclusion of chapter 5, Plomin argues that since there are no disorders, only quantitative dimensions, ‘there is no ‘us’ versus ‘them’.’⁶ His efforts to dismantle the arbitrary line between ‘mental health’ and ‘mental illness’ (that psychiatry draws in order to forcibly ‘treat’ those placed in the latter group) are laudable. But Plomin’s devotion to genetics muddies his message, making it appear contradictory.

Biogenetic Explanations and Their Effects

Another well-intentioned but disputable view expressed by Plomin (in chapter 8 of Blueprint), is that by accepting psychological experiences are (primarily) a consequence of genetic differences, people will become more accepting and less judgmental of both themselves and others who may be suffering.

Rather than blaming other people and ourselves for being depressed, slow to learn or overweight, we should recognize and respect the huge impact of genetics on individual differences. Genetics, not lack of willpower, makes some people more prone to problems such as depression, learning disabilities and obesity. Genetics also makes it harder for some people to mitigate their problems. Success and failure – and credit and blame – in overcoming problems should be calibrated relative to genetic strengths and weaknesses.⁷

This is similar to the idea that viewing ‘mental illness as an illness like any other’ (a belief promoted by SANE Australia⁸and the American Psychiatric Association⁹) reduces the stigma experienced by those diagnosed ‘mentally ill’. This view is generally unsupported by the available evidence (which actually suggests the opposite is true). Whereas evidence for Plomin’s view that understanding the role of genetics can help people feel better about themselves is, at best, mixed.¹⁰

A 2013 meta-analysis ¹¹ found that biogenetic explanations do reduce blame but also induce prognostic pessimism—the view that psychological issues are unlikely to improve and are perhaps permanent—‘set[ting] the stage for self-fulfilling prophecies that could hamper recovery from psychological problems.’¹² This latter finding was reported in an earlier study¹³ whose authors warned that

individuals with a diagnosis of schizophrenia may themselves form deterministic interpretations of the genetic information they receive and subsequently be less likely to adopt behavioural advice or adhere to treatment.¹⁴

More generally, a review of 33 studies¹⁵ examining the relationship between biogenetic explanations and public acceptance of ‘mental illness’ reported that ‘in most instances biological or genetic causal attributions are not associated with lesser rejection of people with mental illness.’¹⁶ A 2010 study also reported that with regards to public causal attributions of ‘schizophrenia’, ‘depression’, and alcohol dependence, although endorsement of biogenetic explanations grew between 1996 and 2006, stigma did not decrease. The researchers concluded: ‘An overreliance on the neurobiological causes of mental illness and substance use disorders is at best ineffective and at worst potentially stigmatizing.’¹⁷

Adopting a biogenetic view may also have implications for therapists and their clients. Research has demonstrated that clinicians with medical training are significantly less empathetic towards individuals diagnosed with ‘schizophrenia’, ‘social phobia’, ‘depression’, and ‘obsessive compulsive disorder’, compared to clinicians without such training.¹⁸ Moreover, biological explanations produce significantly less empathy in clinicians, regardless of training. Finally, a 2015 study found that, compared to psychosocially oriented clinicians, clinicians who framed psychological distress biogenetically were perceived as significantly less warm by all participants.¹⁹ These findings suggest biogenetic explanations pose a threat to the empathic relationship between client and clinician.

Afterword

The research concerning biogenetic explanations and their negative effects could perhaps be downplayed if the data undergirding such explanations were credible. But since psychiatric research is built on invalid assumptions and riddled with confounds, it does not seem accurate to talk of genes causing (or predicting for) ‘schizophrenia’, ‘depression’, or any other psychiatric ‘disorder’, even in the quantitative sense.

Searching for genes that contribute to easily quantifiable traits such as height and weight is one thing, but attempting to do the same for arbitrary categories like ‘schizophrenia’ is an entirely different matter. As psychiatrist Nassir Ghaemi wrote in a 2016 paper²⁰ titled Utility without validity is useless, ‘[i]f we create diagnostic categories based on social, economic and political considerations, why should genes correlate with those categories?’²¹

Plomin said ‘the whole game is to find these people who meet these—what I think are arbitrary diagnostic criteria—and you call them cases, like schizophrenics’, acknowledging that categorising everyone else as a control is ‘simply not true.’ Indeed, it is not true. But neither is the claim that DNA differences predict for ‘schizophrenia’. The arbitrary nature of the ‘game’ being played precludes such a conclusion.

If understanding how genes impact human characteristics is truly the goal, then a new game is needed; one that does not rely on arbitrary lines or labels.

A version of this article was published on August 9, 2020, by Mad in America.

1. Plomin, R. (2018). Blueprint: How DNA makes us who we are. London: Allen Lane.
2. Plomin, 2018.
3. Plomin, 2018.
4. Plomin, 2018.
5. Plomin, 2018.
6. Plomin, 2018.
7. Plomin, 2018.
8. SANE Australia. (2016, December 5). Fact vs myth: mental illness basics. Retrieved May 25, 2020, from SANE Australia: https://www.sane.org/mental-health-and-illness/facts-and-guides/fvm-mental-illness-basics
9. American Psychiatric Association. (2015, November). What is mental illness? Retrieved May 25, 2020, from American Psychiatric Association: https://www.psychiatry.org/patients-families/what-is-mental-illness
10. Haslam, N., & Kvaale, E. P. (2015). Biogenetic explanations of mental disorder: The mixed-blessings model. Current Directions in Psychological Science, 24(5), 399-404. doi:10.1177/0963721415588082
11. Kvaale, E. P., Haslam, N., & Gottdiener, W. H. (2013). The ‘side effects’ of medicalization: A meta-analytic review of how biogenetic explanations affect stigma. Clinical Psychology Review, 33(6), 782-794.
12. Kvaale et al., 2013, p. 782.
13. Bennet, L., Thirlaway, K., & Murray, A. J. (2008). The stigmatising implications of presenting schizophrenia as a genetic disease. J Genet Counsel, 17, 550–559. doi:10.1007/s10897-008-9178-8
14. Bennet et al., 2008, p. 550.
15. Angermeyer, M. C., Holzinger, A., Carta, M. G., & Schomerus, G. (2011). Biogenetic explanations and public acceptance of mental illness: systematic review of population studies. The British Journal of Psychology, 199, 367-372. doi:10.1192/bjp.bp.110.085563
16. Angermeyer et al., 2011, p. 369.
17. Pescosolido, B. A., Martin, J. K., Long, J. S., Medina, T. R., Phelan, J. C., & Link, B. G. (2010). “A disease like any other”? A decade of change in public reactions to schizophrenia, depression, and alcohol dependence. American Journal of Psychiatry, 167(11), 1321-1330, p. 1327.
18. Lebowitz, M. S., & Ahn, W. K. (2014). Effects of biological explanations for mental disorders on clinicians’ empathy. Proceedings of the National Academy of Sciences, 111(50), 17786-17790.
19. Lebowitz, S, M., Ahn, W., & Oltman, K. (2015). Sometimes more competent but always less warm: Perceptions of biologically oriented mental-health clinicians. International Journal of Social Psychiatry, 1-9. doi:10.1177/0020764015573086
20. Ghaemi, S. N. (2016). Utility without validity is useless. World Psychiatry, 15(1), 35-36. doi:10.1002/wps.20287
21. Ghaemi, 2016, p. 36.