Attention deficit hyperactivity disorder is the most commonly diagnosed psychiatric illness in US school children. According to the most recent CDC report, 11% of kids between the ages of 4 and 17 have been diagnosed with ADHD at some point in their lives.
Research suggests that ADHD and ADDers may have lower-than-average levels of dopamine, the neurotransmitter that helps us zero-in on important things around us. ADHD is usually treated using stimulants, like amphetamines, that are classified as Schedule II drugs alongside methamphetamines and morphine.
These medications, like Adderall, Concerta, and Focalin, spike their users’ dopamine levels, which allows them to tune out buzzing peripheral details that otherwise vie for attention.
ADHD is characterized by inattention, hyperactivity, and impulsivity. According to Yale associate professor of public health, Dr. Jason Fletcher, adults with persisting childhood ADHD are “much less likely to be employed at age thirty, and those who [have] jobs [earn] over thirty percent less each year than individuals who [are] not diagnosed with ADHD.”
Outside structured settings, however, the apparent curse can actually be a blessing. Thomas Edison is the historical poster boy for retrospectively-diagnosed ADHD. An inquisitive but unfocused student, he was branded “addled” and dull by his grade school teacher. Edison lasted three months in grade school before his mother insisted on homeschooling him. Free to pursue his insatiably varied interests at home, Edison read voraciously while honing his mechanical and chemical skills.
David Neeleman, the founder and head of JetBlue Airways, is a proud ADDer. Though he barely scraped by in college, the CEO now uses his disorder as an asset. “If someone told me you could be normal or you could continue to have your ADD, I would take ADD,” says Neeleman. “My ADD brain naturally searches for better ways of doing things.”
So if the three pillars of ADHD (inattention, hyperactivity, and impulsivity) equal creativity, energy, and curiosity in less rigid settings, why do we characterize these traits as a disorder? A new neurological study conducted by Washington University’s Dr. Dan T.A. Eisenberg suggests a biological justification for the retention of these traits in our collective gene pool, despite their clash with structured lifestyles. Dr. Eisenberg examined genetic differences among nomadic and settled factions of Ariaal tribesmen in northern Kenya.
Specifically, the research correlated nourishment and the presence of the DRD4/7R allele, which is linked to ADHD and codes for a less sensitive dopamine receptor. Among roaming nomads with a dynamic lifestyle, those with the less responsive receptor were better nourished. Settled and organized farmers, on the other hand, were better nourished if they lacked the insensitive receptor gene.
For individuals who flit smoothly between changing landscapes, ADHD can be an evolutionary advantage. Like the agrarian Ariaal lifestyle, our lives are generally structured, so it’s no surprise that the disorder is at odds with many of our activities. In school especially, ADHD symptoms can be disruptive and derailing to teachers organizing a regimented curriculum for their classes. But when a round peg doesn’t fit a square hole, which one needs to change?
Susan Bodiker / January 23, 2015
Since a dopamine deficiency has been identified as cause of ADD/ADHD, is there any work being done to develop a dopamine-boosting drug to mitigate this condition? Could certain drugs for Parkinson’s Disease be tested, adjusted or prescribed to these individuals?
I have a personal interest in this because my son (very creative!) was diagnosed with ADD when he was in third grade and took Adderall for many years.(although he’s not taking it now). It managed the worst of his symptoms but it’s certainly not harmless. Behavior modification is key but maybe the addition of a new class of drug might make a positive difference too.
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laracheslow / January 24, 2015
Hi Susan,
There have been some studies performed looking into Parkinson’s drugs like L-dopa as potential ADD medications. Unfortunately, research hasn’t yielded any promising results for this route.
There is a key difference between how amphetamines and drugs like L-dopa enhance dopamine function that may explain why Parkinson’s drugs are ineffective. In ADD, the dopamine transporter (DAT) is faulty, which normally pumps dopamine from one neuron into the next. Drugs like amphetamines temporarily patch up the DAT, which can then better shuttle dopamine and raise its accumulated levels in the end neuron. L-dopa, on the other hand, increases dopamine in the brain between neurons. This works for people with Parkinson’s who are deficient in dopamine receptors because each sparse receptor has more chemical to respond to. But having more dopamine available to transport won’t necessarily help ADDers focus if the import mechanism to neurons is still impaired.
I hope this answers your question. Good luck to you and your son!
Lara Cheslow
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Susan Bodiker / January 24, 2015
Thanks, Lara. That makes perfect sense–even to me, a non-medical professional!
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