I wrote this post on September 8, 2009 but it remains important. On that day, a major study in a major journal providing more evidence: ADHD is biological. Beyond the research findings, I share what we rarely see years later: A string of news outlets accurately reporting the story.
You see, in 2009, ADHD clickbait was not yet the lucrative marketing tactic that it is now. Times have changed. I leave it here to provide contrast. Also, because it is a pivotal study.
The headlines this week may not come as news to us. But, following the recent ADHD Hall of Shame entry, science-based reportage comes as welcome relief. The following news sources, among others, report the latest study by NIDA Director Nora Volkow and colleagues showing that, well, ADHD is real. Read all about it.
Headlines Reporting the Research
Here’s a sampling of the breaking headlines, followed by the press release from the researcher:
BBC News: ADHD Brain Chemistry Clue Found
US researchers have pinned down new differences in the brain chemistry of people with attention deficit hyperactivity disorder (ADHD). They found ADHD patients lack key proteins which allow them to experience a sense of reward and motivation.
The Brookhaven National Laboratory study appears in the Journal of the American Medical Association. It is hoped it could help in the design of new ways to combat the condition.
For far too long there has been an assumption that children with ADHD are deliberately wilful
Previous research looking at the brains of people with ADHD had uncovered differences in areas controlling attention and hyperactivity.
Atlanta Journal Constitution: Motivation May Be at Root of ADHD
(HealthDay News) — The trouble concentrating that affects people with attention-deficit hyperactivity disorder (ADHD) might be related to motivation, a new study has found.
The motivational problems seen with the condition, which is often associated with children but can persist into adulthood, appear to stem from a reduction in dopamine, an important neurotransmitter in the nervous system that is considered a hallmark of ADHD.
“ADHD is traditionally a disease where people think the disruption is in attention and hyperactivity,” said Dr. Nora D. Volkow, director of the U.S. National Institute on Drug Abuse and lead researcher on the study. “So, the whole focus on research and treatment has been on attention — with kids who cannot pay attention or are hyperactive.”
CBC News: ADHD study links chemical to symptoms
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Classic symptoms of attention deficit hyperactivity disorder, including inattention and the lack of impulse control, might be caused by a disruption of a chemical in the brain that helps cells communicate, a U.S. study suggests.
Studies have already indicated that dopamine, a neurotransmitter needed for normal functioning of the central nervous system, is disrupted in some pathways of the brain in people with ADHD.
A problem in the brain’s reward center may be behind symptoms like inattention associated with attention deficit …
abc7news.com: Researchers may have found ADHD cause
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BERKELEY, CA (KGO) — Treating attention deficit hyperactivity disorder can be a life-long ordeal, but some researchers believe they may…
Brookhaven National Laboratory
Press release: September 8, 2009
UPTON, NY — A brain-imaging study conducted at the U.S. Department of Energy’s (DOE) Brookhaven National Laboratory provides the first definitive evidence that patients suffering from attention deficit hyperactivity disorder (ADHD) have lower-than-normal levels of certain proteins essential for experiencing reward and motivation.
“These deficits in the brain’s reward system may help explain clinical symptoms of ADHD, including inattention and reduced motivation, as well as the propensity for complications such as drug abuse and obesity among ADHD patients,” said lead author Nora Volkow, Director of the National Institute on Drug Abuse and a long-time collaborator on neuroimaging research at Brookhaven Lab.
JAMA Published Study
The study, published in the September 9, 2009, issue of the Journal of the American Medical Association, also has important implications for treatment. “Finding ways to address the underlying reward-system deficit could improve the direct clinical outcome of ADHD, and potentially reduce the likelihood of other negative consequences of this condition,” said study co-author Gene-Jack Wang, chair of Brookhaven’s medical department.
Prior to this study, it was not clear whether people with ADHD had abnormalities in the brain’s dopamine-mediated motivation/reward system. Previous studies were relatively small. Most were complicated by the fact that some ADHD patients had undergone treatments or had a history of drug abuse or other conditions that can affect the dopamine system.
To strengthen the statistics and control for these factors, the current study looked at 53 adult ADHD patients who had never received treatment and 44 healthy control subjects. All were carefully screened to eliminate potentially confounding variables. The scientists used positron emission tomography (PET) to measure two markers of the dopamine system:
- Dopamine receptors, to which the chemical messenger binds to propagate the “reward” signal, and
- Dopamine transporters, which take up and recycle excess dopamine after the signal is sent.
PET Scans Target Dopamine Transmission
Lying in a PET scanner, each patient was injected with a minute amount of a “radiotracer” compound. That’s a chemical labeled with a radioactive form of carbon and designed to bind specifically to one of the targets. Different tracers were used for each target, and patients were scanned for each at separate times. By detecting the signal from the radiotracers, the PET machine can measure the receptor and transporter locations and concentrations in various parts of the brain.
The results clearly showed that, relative to the healthy control subjects, the ADHD patients had lower levels of dopamine receptors and transporters in the accumbens and midbrain. Those two key brain regions directly affect processing motivation and reward. In addition, the measurements of dopamine markers correlated with measures of behavior and clinical observations of ADHD symptoms. This included reduced levels of attention as measured by standard psychological tests.
Dopamine Reward Pathway
“Our findings imply that these deficits in the dopamine reward pathway play a role in the symptoms of inattention in ADHD and could underlie these patients’ abnormal responses to reward,” Volkow said.
“This pathway plays a key role in reinforcement, motivation, and in learning how to associate various stimuli with rewards,” she continued. “Its involvement in ADHD supports the use of interventions to enhance the appeal and relevance of school and work tasks to improve performance.
“Our results also support the continued use of stimulant medications — the most common pharmacological treatment for ADHD — which have been shown to increase attention to cognitive tasks by elevating brain dopamine,” she said.
Findings Help Explain Addiction Risk
The findings may also help explain something else: why ADHD patients are more likely than control subjects to develop drug-abuse disorders and conditions such as obesity.
Other studies from our group suggest that patients who abuse drugs or overeat may be unconsciously attempting to compensate for a deficient reward system by boosting their dopamine levels. Understanding how deficits in the dopamine system contribute to ADHD and finding ways to improve the functioning of the reward system could help mitigate these troubling consequences in the ADHD patient population.
This research was supported by the National Institute on Alcohol Abuse and Alcoholism Intramural Research Program and by the National Institute on Mental Health. The Office of Biological and Environmental Research within DOE’s Office of Science provides infrastructure support for the radiotracer chemistry and imaging facilities at Brookhaven Lab. Brain-imaging techniques such as PET are a direct outgrowth of DOE’s long-standing investment in basic research in chemistry, physics, and nuclear medicine.
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