Use of stimulants for attention deficit hyperactivity disorder: FOR

As one might expect with an author with such obvious conflicts of
interest, Dr Coghill fails to engage the diverse interdisciplinary
literature on ADHD and presents a very narrow bio-medical view of the
existing scientific evidence. His arguments reach unwarranted conclusions
at every stage. With regards the biological underpinnings of ADHD, it is
indeed impressive how much biological research has been carried out into
this apparent medical condition for so little return. The problem for
those who believe that ADHD is a discrete medical condition is that as
soon as you get into specifics their arguments start to fall apart. Thus
it is argued that molecular genetic variations have been robustly
replicated, concluding that ADHD is associated with the dopamine
transporter gene (DAT1) and the dopamine receptor gene (D4) (Schachar and
Tannock, 2002), yet a recent study of 126 sibling pairs concluded that
these two genes if they are involved in ADHD aetiology at all, make only a
minor contribution to overall genetic susceptibility (Fisher et al, 2002).
With regards physical counterparts in brain structure of children with
ADHD, one wonders how there can be known physical counterparts if there is
yet to be a study that compares unmedicated children with an age matched
control group, with the largest study that claimed to have done this
(Castellanos et al, 2002) choosing a control group whose age was on
average 2 years older (Leo and Cohen, 2003) and thereby all they
scientifically managed to prove was that younger children had smaller
brains than older ones! They had a large control group and one wonders why
they decided not to use a straightforward age-matched control group.

Despite claims for the miraculous effects of stimulants they are not
a specific treatment for ADHD, because they are well known to have similar
effects on otherwise normal children and other children regardless of
diagnosis (Breggin, 2002; Rapoport et al., 1978), nor is there any
evidence to show that they have any long lasting beneficial impact
(Timimi, 2002). A more recent meta-analysis of randomized controlled
trials of methylphenidate than the one Dr Coghill cited, found that the
trials were of poor quality, there was strong evidence of publication
bias, short-term effects were inconsistent across different rating scales,
side effects were frequent and problematic and long-term effects beyond 4
weeks of treatment were not demonstrated (Schachter et al, 2001).

The potential long-term adverse effects of giving psychotropic drugs
to children need to cause us more concern than the author will allow.
Stimulants are potentially addictive drugs with cardiovascular, nervous,
digestive, endocrine, and psychiatric side effects and occasionally cause
death (Breggin, 2002, see also www.ritalindeath.com). With regard to
future stimulant abuse, Dr Coghill failed to mention Professor Lambert’s
work that the pro-ADHD lobby has been trying to marginalize. Her study (in
press) drew on longitudinal data from the largest population of ‘ADHD’
children (nearly 500) with age-matched controls, followed for the longest
number of years (on average until they were 27 years old) than any of the
studies purporting to show that stimulants do not lead to future substance
abuse. Lambert found that childhood use of stimulant treatment is
significantly and pervasively implicated in the uptake of regular smoking,
in daily smoking in adulthood, in cocaine dependence, and lifetime use or
abuse of cocaine and stimulants (see for example
www.psychiatrictimes.com/p991201b.html). At a psychological level the use
of drug treatment scripts a potentially life-long story of disability and
deficit that physically healthy children may end up believing. Children
may view drug treatment as a punishment for naughty behaviour and may be
absorbing the message that they are not able to control or learn to
control their own behavior. Drug treatment may also distance all concerned
from finding more effective, long-lasting strategies. The child and their
carers may be unnecessarily cultured into the attitude of a “pill for
life’s problems” (Timimi et al, 2004).

The MTA study that Dr Coghill cites as a good reason to recommend
that stimulants be given as a first line treatment sets a dangerous
precendent in its conclusion that medication is better than psych-social
therapies. This study has been widely criticised on many grounds,
including lack of placebo group or blinding, authors being firm advocates
of ADHD and well known reciepiants of drug company money, playing down of
the numbers of children experiencing side-effects, participants already
being ‘cultured’ into believing the children involved had a biological
condition, study only lasting 14 months, and the fact that two thirds of
those in the poorest outcome group (community treatment) were taking the
very same stimulants.

This gun-ho approach to evaluating the evidence for the use of
stimulants will benefit only the pockets of the drug companies and raises
serious ethical questions for our profession to consider. If other less
problematic and reasonably effective interventions for ADHD-type
behaviours when they are seriously problematic exist (such as family
therapy, diet and other lifestyle interventions, educational, behavioural
and psychodynamic therapies) (Timimi, 2004), should they not be tried
first, even if they are not as quick or perfect? Finally if the argument
of critics such as me, that there is no such thing as ADHD in the first
place proves to be correct (as the evidence currently indicates) what does
this says about the social and political role our profession is
performing? Will future generations forgive us for colluding, by our
‘dumbing down’ millions of healthy youngsters exuberant behaviours, with
Western culture’s hostility children (particularly boyhood), because we,
as a society, are deciding that we can no longer tolerate the diversity,
and joyful unpredictability that children bring?

References:

Breggin, P. (2002). The Ritalin fact book. Cambridge, MA: Perseus

Castellanos, F. X., Lee, P. P., Sharp, W., et al (2002) Developmental
trajectories of brain volume abnormalities in children and adolescents
with attention-deficit/hyperactivity disorder. Journal of the American
Medical Association, 288, 1740 -1748

Fisher, S.L., Francks, C., McCracken, J.T., et al (2002). A genome-
wide scan for loci involved in Attention Deficit/Hyperactivity Disorder
(ADHD). American Journal of Human Genetics, 70, 1183-1196.

Leo, J.L., & Cohen, D.A. (2003). Broken brains or flawed studies?
A critical review of ADHD neuroimaging research. The Journal of Mind and
Behavior, 24, 29-56.

Rapoprt, J. L., Buchsbaum, M. S., Zahn, et al (1978).
Dextroamphetamine: Cognitive and behavioral effects in normal prepubertal
boys. Science, 199, 198–214.

Schachar, R., & Tannock, R. (2002). Syndromes of hyperactivity
and attention deficit. In Child and Adolescent Psychiatry (4th Edition) M.
Rutter & E. Taylor (eds), pp399-418. Oxford: Blackwell.

Schachter, H., Pham, B., King, J., et al (2001). How efficacious and
safe is short-acting methylphenidate for the treatment of attention-
deficit disorder in children and adolescents? A meta- analysis. Canadian
Medical Association Journal, 165, 1475–1488.

Timimi, S. (2002). Pathological child psychiatry and the
medicalization of childhood. Hove, UK: Brunner-Routledge.

Timimi, S. (2004) Helping children who could be diagnosed with ADHD
and their families: Oscillating between modernist and post-modernist
perspectives. Clinical Psychology 40, 24-26.

Timimi, S. & 33 co-endorsers (2004a). A critique of the
international consensus statement on ADHD. Clinical Child and Family
Psychology Review 7, 59-63.

Competing interests:
None declared