For readers of in my article, I note that there is now substantial published evidence which suggests that stimulant medications such as Adderall, Vyvanse, Concerta, Metadate, Focalin, and Daytrana may damage the nucleus accumbens, the motivational center of the brain. On this page, I provide some of the evidence which supports that statement.


Professor William Carlezon and his colleagues at Harvard Medical School were among the first to report that when they gave stimulant medications - such as those used to treat children who have been diagnosed with ADHD - to young laboratory animals, the result was that those animals displayed a loss of drive when they grow up.[1] These animals look normal, but they are lazy. They do not want to work hard for anything, not even to escape a bad situation.

The Harvard investigators suggested that the stimulant medications might cause a similar phenomenon in children. Children who take these medications may look fine while they are taking them. They may look fine after they stop taking them. But when they are no longer taking the medication, they will not have much drive. They will not have much get-up-and-go.

The stimulant medications appear to exert their harmful effects by damaging an area in the developing brain called the nucleus accumbens, both in humans and in laboratory animals.[2] For neuroscientists, that is not much of a surprise. All these medications work by mimicking the action of dopamine, and the nucleus accumbens has a high concentration of dopamine receptors.[3] If you give any of these medications to a child, the medication is likely to bind to receptors in the nucleus accumbens, which may disrupt the development of the nucleus accumbens.

The nucleus accumbens is the motivational center of the brain.[4] More precisely, the nucleus accumbens is the part of the brain that is responsible for translating motivation into action. If the nucleus accumbens is damaged, a child may still feel hungry. But she or he just will not feel motivated to do much about it. If you damage the nucleus accumbens, the result is likely to be less motivation, less engagement, less drive to achieve in the real world. That may be the end result of long-term use of medications such as Adderall, Ritalin, Concerta, Metadate, Focalin, Daytrana, or Vyvanse.

Many of the studies cited here are based on research in laboratory animals, not in humans. But researchers have now documented that stimulant medications prescribed for ADHD actually shrink the nucleus accumbens and related structures in the human brain, although some of these changes may be transient, at least in some individuals.[5] Other researchers have found that even occasional use of these medications results in changes in the structure of the brain.[6]

The evidence that stimulant medications appear to shrink the nucleus accumbens in humans is especially disturbing in light of research which documents a nearly linear correlation between the volume of the nucleus accumbens and individual motivation. These studies suggest that the smaller the nucleus accumbens, the more likely that person is to be apathetic, lacking in drive.[7]

When I rattle off that list of medications - Adderall, Ritalin, Concerta, Metadate, Focalin, Daytrana, and Vyvanse - you may think that I am talking about seven different medications. In fact, I am talking about just two medications: amphetamine and methylphenidate. Adderall and Vyvanse are proprietary blends of amphetamine. Ritalin, Concerta, Focalin, Metadate, and Daytrana are each a proprietary version of methylphenidate.

Can we say 100% for sure that these medications cause lasting injury to the brain? Of course not. It is very difficult to say anything in medicine 100% for sure. But our job, as parents, requires us to make decisions with less than 100% certainty. If you wait until we know 100% for sure that these medications are dangerous, your child may be middle-aged.

I recommend that you choose a safer alternative. If you are convinced that your child needs a medication for ADHD, then choose a non-stimulant such as Wellbutrin, Intuniv, and Strattera. All medications have risks, but the non-stimulant medications do not pose a risk of damage to the nucleus accumbens. They don’t mimic the action of dopamine.

The Drug Enforcement Administration has classified Adderall, Ritalin, Concerta, Metadate, Focalin, Daytrana, and Vyvanse, as schedule II drugs. Schedule II drugs are considered to have the highest potential for abuse and addiction. (Schedule I drugs, such as heroin, are not legal for clinical use at all.) If you are going to medicate your child, avoid a Schedule II drug except as a last resort. There are, as I said, many safer alternatives. Wellbutrin, Intuniv, and Strattera, are not Schedule II and indeed are not scheduled at all. And in case you are wondering, I have no affiliation with, and I accept no payment from, the companies which manufacture Wellbutrin, Intuniv, and Strattera. 


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This page is adapted from my book The Collapse of Parenting (New York: Basic Books, 2015), pp. 65 – 66 and the accompanying endnotes; and also from my book Boys Adrift (New York: Basic Books, 2009), pp. 89 – 90.


[1] Here are three of the papers which Dr. Carlezon coauthored on this topic:

Enduring behavioral effects of early exposure to methylphenidate in rats, Biological Psychiatry, volume 54, pp. 1330 – 1337, 2003.

Understanding the neurobiological consequences of early exposure to psychotropic drugs, Neuropharmacology, volume 47, Supplement 1, pp. 47 – 60, 2004.

Early developmental exposure to methylphenidate reduces cocaine-induced potentiation of brain stimulation reward in rats, Biological Psychiatry, volume 57, pp. 120 – 125, 2005.

[2] Many scholarly studies have now demonstrated that methylphenidate and amphetamine – the active ingredients in these medications – can cause lasting changes to those areas of the developing brain where dopamine receptors are found. The disrupting effects appear to be centered on the nucleus accumbens, which is not surprising, because, as noted, the nucleus accumbens has a high density of dopamine receptors. Terry Robinson and Bryan Kolb at the University of Michigan were among the first to demonstrate that low-dose amphetamine leads to damage to dendrites in the nucleus accumbens. They first documented this finding in their paper Persistent structural modifications in nucleus accumbens and prefrontal cortex neurons produced by previous experiences with amphetamine, Journal of Neuroscience, volume 17, 8491-8497, 1997. They reviewed this emerging field in their article Structural plasticity associated with exposure to drugs of abuse, Neuropharmacology, volume 47, pp. 33 – 46, 2004. See also Claire Advokat, Update on amphetamine neurotoxicity and its relevance to the treatment of ADHD, Journal of Attention Disorders, volume 11, pp. 8 – 16, 2007.

Other relevant articles include (in alphabetical order):

·       Esther Gramage and colleagues, Periadolescent amphetamine treatment causes transient cognitive disruptions and long-term changes in hippocampal LTP, Addiction Biology, volume 18, pp. 19 – 29, 2013.

·       Rochellys D. Heijtz, Bryan Kolb, and Hans Forssberg, Can a Therapeutic Dose of Amphetamine During Pre-adolescence Modify the Pattern of Synaptic Organization in the Brain? European Journal of Neuroscience, volume 18, pp. 3394–3399, 2003.

·       Yong Li and Julie Kauer, Repeated Exposure to Amphetamine Disrupts Dopaminergic Modulation of Excitatory Synaptic Plasticity and Neurotransmission in Nucleus Accumbens, Synapse, volume 51, pp. 1–10, 2004.

·       Manuel Mameli and Christian Lüscher, 2011: Synaptic plasticity and addiction: learning mechanisms gone awry, Neuropharmacology, 61:1052-1059. 2011.

·       Shao-Pii Onn and Anthony Grace, Amphetamine Withdrawal Alters Bistable States and Cellular Coupling in Rat Prefrontal Cortex and Nucleus Accumbens Neurons Recorded in Vivo, Journal of Neuroscience, volume 20, pp. 2332–2345, 2000.

·       Margery Pardey and colleagues, Long-term effects of chronic oral Ritalin administration on cognitive and neural development in adolescent Wistar Kyoto Rats, Brain Sciences, volume 2, pp. 375 – 404, 2012.

·       Scott Russo and colleagues, The addicted synapse: mechanisms of synaptic and structural plasticity in the nucleus accumbens, Trends in Neuroscience, volume 33, pp. 267 – 276, 2010.

·       Louk J. Vanderschuren and colleagues, A Single Exposure to Amphetamine is Sufficient to Induce Long-term Behavioral, Neuroendocrine, and Neurochemical Sensitization in Rats, Journal of Neuroscience, volume 19, pp. 9579–9586, 1999.

For a thoughtful review of the underlying neurochemistry, the similarities between the prescription stimulant medications and cocaine, and an assessment of the long-term risks for people who take these medications, please see the review by Heinz Steiner and Vincent Van Waes, Addiction-related gene regulation: risks of exposure to cognitive enhancers vs. other psychostimulants, Progress in Neurobiology, volume 100, pp. 60 – 80, 2013. 

[3] There is consensus that methylphenidate works by increasing the action of dopamine in the synapse: see for example Nora Volkow and colleagues, Imaging the effects of methylphenidate on brain dopamine: new model on its therapeutic actions for attention-deficit/hyperactivity disorder, Biological Psychiatry, volume 57, pp. 1410 – 1415, 2005. And it has long been recognized that amphetamine mimics the action of dopamine in the brain, and that the dopamine system is key to ADHD: see for example James Swanson and colleagues, Dopamine and glutamate in attention deficit disorder, pp. 293 – 315 in the book Dopamine and Glutamate in Psychiatric Disorders, edited by Werner Schmidt and Maarten Reith, Humana Press, 2005.  

[4] For more on the central role of the nucleus accumbens in motivation, see Dr. Carlezon’s paper, Biological substrates of reward and aversion: a nucleus accumbens activity hypothesis, Neuropharmacology, 2009, volume 56, Supplement 1, pp. 122 – 132. 

[5]See Elseline Hoekzema and colleagues, Stimulant drugs trigger transient volumetric changes in the human ventral striatum, Brain Structure and Function, volume 219, pp. 23 – 34, 2013. For a recent replication of this finding, see Mónica Franco Emch, Ventro-striatal/nucleus accumbens alterations in adult ADHD: effects of pharmacological treatment. A neuroimaging region of interest study, Universitat Pompeu Fabra, 2015, full text online at 

[6] See Scott Mackey and colleagues, A voxel-based morphometry study of young occasional users of amphetamine-type stimulants and cocaine, Drug and Alcohol Dependence, volume 135, pp. 104 – 111, 2014.

[7] See Nicolas Carriere and colleagues, Apathy in Parkinson’s Disease is associated with nucleus accumbens atrophy: a magnetic resonance imaging shape analysis, Movement Disorders volume 29, pp. 897 – 903, 2014.  See also Robert Paul, Adam Brickman, Bradford Navia, and colleagues, Apathy is associated with volume of the nucleus accumbens in patients infected with HIV, Journal of Neuropsychiatry and Clinical Neuroscience, volume 17, pp. 167–171, 2005.