Culture, ‘Madness’ & Medicalisation: Social and biological perspectives on the rise of ADHD in children in the UK

In our third year Culture, ‘Madness’ and Medicalisation module, students receive a critical introduction to today’s dominant psychological/clinical practices such as psychoanalysis, bio-psychiatry, psychotherapy, counselling and clinical psychology and the importance of anthropology in illuminating how psychological/clinical practices are dramatically shaping contemporary subjectivities and wider socio/cultural life. This year, our featured essay from the module is by Patricia Mitchell – what follows is an abridged version of the piece.
Patricia’s bio: I discovered anthropology 5 years ago whilst volunteering in Nepal and, having completed my undergraduate degree at Roehampton as a mature student, I have thoroughly enjoyed this eye-opening journey.
Patricia Mitchell

The rise of ADHD in children in the UK: biological and social perspectives

The rate of diagnosis for attention deficit hyperactivity disorder (ADHD) in the UK has risen drastically in the last decade (Greenblatt and Delane, 2017).  It is estimated that 1 in 100 UK children between 5 and 16 years old have severe symptoms, rising to 5 in 100 with less severe symptoms (NICE, 2008), which is reported to be a 700% increase during the decade 1990-2000 (Greenblatt and Delane, 2017). ADHD has created controversy in relation to causality, diagnosis and treatment, making it the most thoroughly researched child psychiatric ’disorder’ (Timini, 2004). In what follows, I explore biological and social perspectives on the condition and some of the controversies it has raised.

The biology of ADHD

ADHD first entered the DSM in 1980, diagnosed as ‘the inability to marshal and sustain attention, modulate activity level, and moderate impulsive actions’ (Rappley, 2005, p.165). By the 4thedition in 2000, there were 3 subtypes of ADHD: combined, predominantly inattentive, and predominantly hyperactive-Impulsive.  Today, ADHD is considered to be psychiatry’s ‘number one biologically based disease’ (Visser and Jehan, 2009).

Classified as a neurodevelopmental disorder with abnormal behaviours found across different settings, ADHD is understood to result from an innate biomedical impairment. ADHD is a developmental failure in the brain’s circuitry that underlies inhibition and self-control (Visser and Jehan, 2009).  The majority of research has concentrated on molecular genetics and dysfunctional genes, which are suggested to be the underlying cause.  Neuroimaging tools such as PET and MRI scans compare brain activity of children with a diagnosis of ADHD to family members who don’t (Visser and Jehan, 2009) and studies on twins and adopted children show strong genetic familial links of ADHD.  Hyperactivity tests support this, with full siblings showing higher rates than half siblings (Thapar et al., 1999).  Relatives of children with ADHD also display an increased risk of other psychiatric disorders, such as depression, anxiety and learning disorders.  Comorbidity, having one or more disorders is prevalent in these groups (Thapar et al., 1999).

Correlating the basis of ADHD to an innate biomedical dysfunction justifies pharmacological medication.  First line treatments are psychostimulants, such as methylphenidate (Ritalin and Concerta) and amphetamines.  Their efficacy has been demonstrated in clinical trials, again based on neuroimaging, showing alterations in brain functioning that halt ADHD symptoms.  Volkow and Swanson (cited in Visser and Jehan, 2009) conducted research establishing that amphetamines and methylphenidate, by blocking dopamine transporters from the terminal, increase extracellular dopamine in the brain, replicating the function of the neurotransmitter dopamine by arousing the nervous system.  Large volume changes of dopamine in the frontal regions of the brain within one hour of ingestion restore the brain dysfunction and relieve the symptoms of ADHD (Visser and Jehan, 2009). The results obtained from a MTA study (cited in Visser and Jehan, 2009) indicated that the medication condition was viewed to be a ‘consistent dominant variable’, supporting medical intervention as an effective treatment yielding optimal results. Follow up studies intensified this finding, giving strong empirical basis of effectiveness, verifying that ADHD is a result of an innate biomedical impairment (Visser and Jehan, 2009).

Critical perspectives on biological mechanisms

Critics claim that empirical evidence of neuro-biomedical mechanisms correlated to causality are ‘over-simplified’ and often exaggerated, and insist that no biological abnormality has ever been linked to ADHD. Highlighting discrepancies in neuroimaging studies, Orden and Paap (cited in Visser and Jehan, 2009) claim that PET and MRI scans only measure changes in blood flow and brain activity, reducing behaviour to uncontrolled reactions to stimuli.  Further studies challenge the evidence of abnormalities of dopamine neurotransmission to the pathology of ADHD, claiming there are no specified unified genetic variants that definitely demonstrate a causal contribution to ADHD (Visser and Jehan, 2009).  Moreover, familial transmission of ADHD can be explained by shared environmental factors such as social disadvantage, as well as by genes. Therefore, to examine the genetic contribution to ADHD, additional evidence should be gathered from twin and adoption studies, which distinguish between genetic and environmental effects, such as maternal bias and sibling rivalry (Thapar et al., 1999).

Hyperactivity and ADHD, both used in genetic studies, highlight differences in diagnostic definitions and ignore additional influences in study populations such as: referral bias, age, gender, IQ, degree of comorbidity and socio-economic status. Constraints of certain social demographics, such as poor housing, government benefits, healthcare access and education cannot be overlooked.  Cultural factors of parental status, job insecurity, divorce and breakups have an emotional disruptive effect on children. Working mothers experiencing depression have a significantly higher rate of children suffering from emotional and behavioural disorders (Timimi, 2010).  High levels of lead in drinking water are associated with a four-fold increase in risk for children and ADHD (Greenblatt and Delane, 2017). Toxicity from heavy metals, household and industrial chemicals, smoke and pesticides are also linked to brain cell damage in children with ADHD (Greenblatt and Delane, 2017).

Deficiencies of zinc, iron, magnesium, Vitamins B6 and C are identified in most cases of ADHD.  Many studies have demonstrated improved cognition, mood and behaviour with micronutrient supplements (Greenblatt and Delane, 2017). Trials have shown supplements are comparable to medication with less side effects (Popper, 2017). Zinc deficiency alone is a recognised global concern, with 17% of the world’s population at risk. Zinc plays a key role in enzyme activation, neurotransmitter synthesis and critical for dopamine and serotonin regulation. Evidence confirms a direct correlation of ADHD symptoms to low blood and hair levels of zinc. Tests of school children’s ability to pay attention showed that they increased with zinc supplements, suggesting that zinc levels could be a better biomarker of ADHD (Greenblatt and Delane, 2017).  Common nutritional deficiencies are easily and cheaply rectified.  They can be tailored to individual variations of metabolism, digestion and food sensitivity. Therefore, neglecting this evidence of safe and affordable supplements is personally, socially, and economically unjust (Galler et al., 2012). 

Critiques of the medicalization of ADHD

Despite the efficacy of other approaches,ADHD medication has risen in prescription rates around the world since 1990 and is directly correlated to GDP, reflecting huge drug profitability (Greenblatt and Delane, 2017). The UK prescription rate, in a three-year period (1994-97) rose 15-fold, from 6,000 to 92,000 a year (Greenblatt and Delane, 2017).  By 1999, the prescription rate was 131,000, rising to 345,000 in 2003 (Baldwin, 2000). Psycho-stimulants such as Ritalin are virtually indistinguishable from speed or cocaine (Greenblatt and Delane, 2017).  Children as young as two years old have been prescribed Ritalin (Zito et al, 2000), which has rapid uptake and highly addictive qualities, beneficial only in short term periods, 4 to 5 hours; however, after 4/5 weeks it shows reduced effect and dosage then needs to be increased (Visser and Jehan, 2009). Claims from a number of researchers show that current medication is ineffective in at least half of patients (Greenblatt and Delane, 2017).

The long-term efficacy and safety of psychostimulants is under researched and fears of long term side effects from their toxic properties are continually raised (Visser and Jehan, 2009). Pharmaceutical arguments are that the potential side effects, which could cause permanent and irreversible toxic damage, are outweighed by the short-term positive effects (Travell and Visser 2006).  However, the pressure from parents and educators on psychiatrists and GPs to prescribe psychostimulants raises questions about who actually benefits from the short-term effects (Visser and Jehan, 2009). For example, findings from a MTA study (1999) claiming methylphenidate as a safe and effective treatment for ADHD were based on data from parents and teachers, ignoring the children’s own feelings of effects (Visser and Jehan, 2009).  In the UK, it is now possible to obtain diagnosis by a 25-minute telephone consultation, without the child concerned even being seen by the professional making the diagnosis (Timimi and Radcliffe, 2005).

The escalating use of psychostimulant medication in children as the first line of treatment opens controversies about the medicalisation of undesirable child behaviour.  Behavioural norms and requirements in educational settings label those that do not conform.  Defining a disability requiring special needs is now being shaped by medicine and psychology (Timimi and Radcliffe, 2005).  Children taking stimulants are perceived to be less troublesome, accepting that non-compliant behaviours are caused by a medical condition.  This has led to an increased demand from teachers to refer children to psychiatrists as diagnosis is now the criteria for obtaining additional educational resources (Timimi and Radcliffe, 2005). There are long-term dangers here of educational professionals losing self-belief and skills of developing reflexive, appreciative child management practices alongside children maintaining a disability ‘label’ and possible drug reliance for life.  This ‘tunnel vision’ can affect or create damaging social repercussions and mental health problems.

According to Visser and Jehan (2009), ADHD is a social construct of ‘disorders in society creating disorders in children’.  Dr Mike Shooter, former president of the Royal College of psychiatrists claims that many of the diagnosed children plainly do not have these conditions, but are troublesome children reacting to awful family situations.  But, instead of being listened to, they are labelled with a disorder. These incorrect diagnoses are deeply damaging (Mail Online, 2018), with ‘labelled’ children suffering low self-esteem and consequently achieving fewer academic levels, earning lower incomes and having less successful relationships (Galler et al., 2012).

Rather than being a convenient diagnostic ‘dumping ground’ for teachers, parents, doctors and politicians, ADHD needs to be seen in a social light for what it is: as an effect of difficulties in human relationships and institutions of nurturing healthy, well-behaved children (Timimi, 2004).  A more radical social perspective is that the rise in child diagnosis is creating a deep malaise and hostility to children and is borne from our neo-liberal, individualist and consumer lifestyles where children are just ‘getting in the way’ (Timimi and Radcliffe, 2005).

Conclusion

The social implications of ADHD diagnosis, both short and long term, are seen by sociologists as damaging – as a way to socially control undesirable behaviours. In a neo-liberal, individualistic, consumer society, the ADHD labelling of ‘non-achievers’ (resultant from lazy parents), marginalises sufferers and their families.

ADHD suffering to families and educational professionals, and most of all the child, I suggest, is underplayed.  Coping with an energetic, demanding child who sleeps maybe one in twenty-four hours is gruelling for the best parent in the world. But for the child, who in most cases struggles to vocalise their suffering, it must be terrifying.  Only now are we beginning to hear ADHD medicated children from the 90s vocalise their experience regarding the roller coaster of emotions they endured through drug regimens, and the resultant impairments on their futures.

Could the suffering be of a wider social lens, which we would rather not probe into?   Child poverty, working parents, family break-ups, large class sizes, political attitudes to conformity, institutional child interventions are all major issues that are seemingly impossible to re-evaluate.  Therefore, if investment of time and consideration to children suffering with behavioural issues is ignored then the number of children supressed with medication will surely continue to grow.

 References

 Baldwin, S. (2000). Living in Britain: Why are so many amphetamines prescribed to infants, children and teenagers in the UK. Critical Public Health, 10(4), pp.453-462.

Galler, J., Bryce, C., Zichlin, M., Fitzmaurice, G., Eaglesfield, G. and Waber, D. (2012). Infant Malnutrition Is Associated with Persisting Attention Deficits in Middle Adulthood. The Journal of Nutrition, 142(4), pp.788-794.

Greenblatt, J. and Delane, D. (2017). Greenblatt JM, Delane DD (2017) Micronutrient Deficiencies in ADHD: A Global Research Consensus, J Orthomol Med 32(6). Journal of Orthomolecular Medicine, 32 (6).

Mail Online. (2018). Parents want children to be labelled autistic to excuse their failings. [online] Available at: http://www.dailymail.co.uk/news/article-5370241/Parents-want-children-labelled-autistic.html [Accessed 18 Mar. 2018].

MTA Cooperative Group. A 14-Month Randomized Clinical Trial of Treatment Strategies for Attention-Deficit/Hyperactivity Disorder. (1999). Archives of General Psychiatry, 56(12), p.1073.

Popper, C. (2017). 80.1 Broad-Spectrum Vitamin-Mineral Combinations for Treating Psychiatric Disorders of Youth. Journal of the American Academy of Child & Adolescent Psychiatry, 56(10), p.S119.

Rappley, M. (2005). Attention Deficit–Hyperactivity Disorder. New England Journal of Medicine, 352(2), pp.165-173.

Thapar, A., Holmes, J., Poulton, K. and Harrington, R. (1999). Genetic basis of attention deficit and hyperactivity. British Journal of Psychiatry, 174(02), pp.105-111.

Timimi, S. (2010). The McDonaldization of Childhood: Children’s Mental Health in Neo-Liberal Market Cultures. Transcultural Psychiatry, 47(5), pp.686-706.

Timimi, S. and Radcliffe, N. (2005). The rise and rise of attention deficit hyperactivity disorder. Journal of Public Mental Health, 4(2), pp.9-13.

Timimi, S. (2004). A Critique of the International Consensus Statement on ADHD. Clinical Child and Family Psychology Review, 7(1), pp.59-63.

Timimi, S. (2004). Rethinking childhood depression. BMJ, 329(7479), pp.1394-1396.

Visser, J. and Jehan, Z. (2009). ADHD: a scientific fact or a factual opinion? A critique of the veracity of Attention Deficit Hyperactivity Disorder. Emotional and Behavioural Difficulties, 14(2), pp.127-140.

Zito, J., Safer, D. and Dosreis, S. (2000). Trends in the Prescribing of Psychotropic Medications to Pre-schoolers. JAMA, 283(8), p.1025.

 

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