Kindergartners, college students and retirees have attention-deficit hyperactivity disorder
September 4, 2007
I sometimes joke that I got ADHD in college, like a flu going around the dorm (CDC Diagnostic Criteria, Rosenberg, 1998, Angier, 1991, Kluger, 2005, Gilman, 2005). I became easily distracted, fidgety, sometimes forgetful or inattentive of simple, daily activities and occasionally very restless. Most likely, since the symptoms are few in number and not significantly impairing I was simply noticing the effects of a high-stress, academically-challenging environment navigated on little sleep. Although typically a childhood disease, the symptoms may last until adulthood; for some people with attention-deficit/hyperactive disorder symptoms remain unnoticed until placed in a challenging environment with sudden independence, like college. Furthermore, some people afflicted with ADHD are not diagnosed until even later in life—retirement. The structured, scheduled work life they led for decades was taken away exposing for the first time symptoms they later realized were themes throughout their lives. For many people the impetus to see a doctor about these symptoms was a diagnosis of ADHD in their grandchild followed by their child, as ADHD seems to have a genetic component.
According to the Diagnostic and Statistical Manual for Mental Disorders IV there are three types of ADHD (CDC Diagnostic Criteria, CDC What is ADHD, Angier, 1991, Angier, 1994, Moffitt, 2007). One, the predominantly inattentive type, comprised of symptoms such as carelessness, distraction, forgetfulness, trouble organizing, following instructions or completing tasks that require attention or mental effort for long periods of time and inability to keep track of objects. Two, the predominantly hyperactive type, comprised of symptoms such as trouble waiting one’s turn or keeping still, frequent interrupting and excessive talking, restlessness and difficulty remaining quiet. And three, the combined type if criteria are met for both inattentive and hyperactive types. Interestingly, the discrepancy between American and European diagnostic statistics is likely due to a difference in diagnosis. European children typically need to be type three ADHD, the combined type, before being diagnosed. When the same standards are applied to subjects the rates of diagnosis between the continents equalizes, although there are still pockets of higher or lower diagnosis due to awareness and diligence of parents and treating physicians. Although some tests, such as for eye movement and coordination can be more sensitive, the predominant observational method of diagnosis illustrates the inherent subjectiveness and need for a biological method of diagnosis. Strep throat can be diagnosed definitively by a bacterial culture from a throat swab but ADHD has no such concrete method. The personal and cultural standards of proper behavior and impairing behavior color diagnosis and even acceptance of the condition as a disability. For example, many Asian cultures turn a blind eye to mental disorders such as ADHD and instead provide harsher discipline to the afflicted child. On the other hand, the US has seen a trend of overdiagnosis, particularly in boys, because of the characteristic “boys will be boys” behavior that is so similar to ADHD symptoms.
ADHD affects approximately 3-7% of children in the United States (three-quarters of whom are boys) (CDC Research Agenda, CDC What is ADHD, CDC A Public Health Perspective, CDC Injuries and ADHD, CDC Peer Relationships and ADHD, CDC Other Conditions Associated with ADHD, Hersey, 1996, Angier, 1991, Angier, 1994, Wallis, 2006, Kluger, 2005, Kluger, 2003, Harding, 2003, das Neves, 2006, Eisenberg, 2007). About half of these children have another behavioral or learning disorder that can complicate diagnosis and treatment. The ADHD child may have trouble making friends, be accident prone, and have trouble in school despite adequate intelligence. The ADHD child may also have more difficulty identifying dangerous situations, like crossing the street and may need to have distractions such as music or TV removed in order to do homework. Adults with ADHD may have trouble concentrating while driving, keeping a job or be more susceptible to drug addiction. On top of this, families must decide with their physician whether or not to put the child on medication (2.5 million children and 1.5 million adults are medicated for ADHD), rely on behavioral therapy and counseling alone, or substitute alternative treatments like the Feingold diet (artificial additives are removed and certain minerals, amino acids and other supplements are added) for medication. Oddly, a good night’s sleep may be enough to alleviate ADHD symptoms and help the child stay on medication. Approximately twice as many children with ADHD also have sleeping disorders, compared to children without ADHD. Poor sleep not only exacerbates ADHD symptoms but also presents some of the same symptoms, much as I saw in college, that could be misdiagnosed as ADHD.
It is unlikely that the apparent rise in ADHD diagnosis is due to a new cause of ADHD (or lax parenting) but to better diagnosis and establishment of the condition itself (Eisenberg, 2007, Hersey, 1996, Angier, 1994, Harding, 2003). The major debates surrounding ADHD, is it overdiagnosed and is it overmedicated, are based on one fact: the cause of ADHD is unknown. With no physical explanation for ADHD no absolute diagnostic criteria can be established and no mechanism for treatment can be explained. The current treatment of amphetamines, such as Ritalin, is based on 7 decades of observation of changed behavior but little else. Similarly, the Feingold diet is based on observed behavioral changes and has been shown by some studies to be as effective as Ritalin in some children, although no cellular explanation can be given for either treatment. Both are based on the theory that the brain cells are not signaling properly and the addition of an amphetamine (Ritalin) or removal of preservatives and artificial additives together with specific supplements (Feingold diet) restore the correct brain function or bypass the missing signaling component. Until a definitive cause of ADHD and resulting treatment are found there will continue to be underdiagnosed and overdiagnosed (and overmedicated) children simply because of different standards of behavior and unruliness and limited spread of more sensitive tests.
CDC ADHD Diagnostic Criteria: http://www.cdc.gov/ncbddd/adhd/symptom.htm
CDC ADHD Research Agenda: http://www.cdc.gov/ncbddd/adhd/dadagenda.htm
CDC What is ADHD?: http://www.cdc.gov/ncbddd/adhd/what.htm
CDC ADHD A Public Health Perspective: http://www.cdc.gov/ncbddd/adhd/publichealth.htm
CDC Injuries and ADHD: http://0-www.cdc.gov.mill1.sjlibrary.org/ncbddd/adhd/injury.htm
CDC ADHD Peer Relationships and ADHD: http://www.cdc.gov/ncbddd/adhd/peer.htm
CDC ADHD Other Conditions Associated with ADHD: http://www.cdc.gov/ncbddd/adhd/otherconditions.htm
Hersey, Jane. Diets and Drugs for Disruptive Children. The New York Times. 1996.
Rosenberg, Merri. Strategies to Manage a Disorder. The New York Times. 1998.
Angier, Natalie. Kids Who Can’t Sit Still. The New York Times. 1991.
Angier, Natalie. The Nation; The Debilitating Malady Called Boyhood. The New York Times. 1994.
Wallis, Claudia. Getting Hyper about Ritalin. Time Magazine. 2006.
Kluger, Jeffrey. Medicating Young Minds. Time Magazine. 2003.
Kluger, Jeffrey. Sleep Deprivation and ADHD. Time Magazine. 2005.
Gilman, Lois. All Jumbled Up. Time Magazine. 2005.
Moffitt, Terrie E. and Maria Melchior. Why does the worldwide prevalence of childhood attention deficit hyperactivity disorder matter? American Journal of Psychiatry, Vol. 164, No. 6. 2007.
Harding, Karen L. et al. Outcome-based comparison of Ritalin versus food-supplement treated children with ADHD. Alternative Medicine Review. Vol. 8, No. 3. 2003.
das Neves, Sergio and Rubens Reimao. Sleep disturbances in 50 children with attention-deficit hyperactivity disorder. Arquivos de Neuro-Psiquiatria. Vol. 65, No. 2-A. 228-233. 2007.
Eisenberg, Leon. Commentary with a historical perspective by a child psychiatrist: When “ADHD” was the “brain-damaged child.” Journal of Child and Adolescent Psychopharmacology. Vol. 17, No. 3. 2007.
Although published observations of autistic behavior date back to the 18th century it was not until 1943 that that disease was named (CDC). At that time Dr. Leo Kanner conducted a study of 11 children noting “autistic disturbances of affective contact”. The term autistic was coined about 30 years before to describe a condition marked by “a tendency to view life in terms of one’s own needs and desires”.(Random House Unabridged Dictionary) Around the same time Dr. Hans Asperger completed a study of 400 children noting similar behavior (CDC). The result was the classification of Autistic Spectrum Disorders (ASD) including autistic disorder, Asperger’s Syndrome, and pervasive developmental disorder-not otherwise specified. ASDs affect approximately 1 in 150 children in all races, ethnicities and socioeconomic groups equally (CDC, Beaudet, Maimburg, Cantor, Nagarajan). Autism is four times as likely to affect males as it is to affect females.
Autism is a developmental disability that is not related to intellectual capacity (CDC, Beaudet, Maimburg, Cantor, Nagarajan). Children affected with autism have difficulty with social interaction, communication, relating and understanding feelings and sensations, and paying attention. Autistic children may also have different ways of learning and may accomplish harder tasks, such as multiplication or reading words, before easier tasks such as number identification or letter pronunciation. Children with autism may be uncomfortable being touched and prefer solitude and undeviating routines and repetitive behaviors. A difficulty identifying appropriate feelings in a situation, personal space, body language and tone of voice are also symptoms common in ASDs. Verbal skills range from no language skills to relatively normal language skills although a person with an ASD may not recognize the natural ebb and flow of a conversation and stick to one personal topic for long periods of time. ASD symptoms are limited to social interaction and communication skills although they may be present along with another disorder such as mental retardation, epilepsy, Fragile X syndrome, tuberous sclerosis, congenital rubella syndrome or untreated phenylketonuria. Asperger’s syndrome is usually differentiated as a mild version of autism although the range of abilities and spectrum of symptoms in autistic disorder can be quite broad.
Since the symptoms for ASDs are so wide ranging it is important for infants and toddlers to complete standard screening tests (CDC). One-third to one-half of parents with autistic children notice symptoms by the child’s first birthday, with 80-90% noticing symptoms by the second birthday. The child may not have any difficulty with walking or other motor skills and show an ability to complete puzzles or other intellectual activities on par with their age group but they may not be able to play pretend or focus on objects or people. The child may also stop gaining skills or lose skills as a toddler. Early screening tests will help to identify those symptoms that may suggest autism (most children are diagnosed by age 4-5) in time to start behavioral therapies, currently the only treatment for ASDs. Some doctors may suggest talking to a nutritionist about diet changes that can help control symptoms and behavior. Similarly, some benefits have been seen with massage therapy, homeopathy, dance, or meditation. It is important to discuss alternative therapies with a doctor to prevent malnutrition or potentially harmful therapies. Currently, about one-third of autistic patients receive an alternative therapy although up to 10% may be harmful. Medication may also be given to control hyperactive energy levels, depression, seizures, attention deficiencies, or self-injurious behavior that frequently occur with autism or linked disorders.
ASDs are described as highly heritable although the genetic basis is unknown (CDC, Beaudet, Nagarajan). Simply put, a person with an autistic disorder may pass the condition to their child but may not have inherited the disease from a parent. De novo, or new, mutations occur in a number of genes that have been shown to be linked to autism (about 10-20% of cases). These mutations may be caused by environmental factors, although those are largely unknown. Another way of looking at ASD inheritance can be shown in twin studies. With identical twins, one twin affected with an ASD means the other has a 75% chance of being affected. A fraternal twin, however, has only a 3% chance of being affected if their twin is affected. Similarly, if a family has one child with an ASD there is a 2-8% chance of the second pregnancy producing a child with autism. Finding a genetic cause can be complicated. The cause may or may not be inherited. It may or may not be the result of a genetic mutation or environmental cause in the womb (thalidomide, for example). What other factors can contribute to ASDs if genetics and environment do not account for all the cases? Some cases can be explained by a different kind of change to DNA, what is called an epigenetic change. Genetic changes to DNA are considered changes to the sequence of DNA by deletion, duplication or base-pair change. Epigenetic changes to the DNA cover the way DNA is packaged in a cell’s nucleus. Each cell contains about 6 feet of DNA, clearly too much to fit in a cell without a highly-regulated packaging method (Hypertextbook). (Since every body has about 10 trillion cells the total DNA in every person can make about 70 trips to the sun and back). One method is called methylation and basically winds the DNA so tightly that the genes can not be expressed (CDC, Beaudet, Nagarajan). Methylation is common in cancer cells where most genes are hypomethylated, or turned on, while tumor suppressor genes (the brakes on tumor development) are hypermethylated. What this means for autism and other psychiatric disorders is that some genes the brain cells need for normal function are perfectly normal but locked away. One such gene can cause enough disruption to the brain to cause autism, schizophrenia or other psychiatric disorders. Altered methylation patterns have been linked to autistic patients with older fathers (Cantor) and some cases of assisted reproduction (such as IVF) (Maimburg); although, one study shows a decreased chance of autism after the rise of assisted reproduction. This study accounts for the cases where the assisted reproduction caused altered methylation. While it is not always known how methylation patterns in the brain cells are altered it is thought to occur early in development. Diagnostic tests are in development to identify these patients (Nagarajan). Likewise, drugs to undo methylation are in development and may be used to treat these subset of patients.
Not all cases of autism can be explained and no one explanation covers all cases. The broad range of symptoms and abilities in autistic patients is reflected in the many cellular causes of autism. Currently the best treatment for children with an ASD is an early diagnosis and behavioral intervention with medical treatment for those symptoms that require it.
Centers for Disease Control, http://www.cdc.gov/ncbddd/autism
Random House Unabridged Dictionary, Random House, Inc, 2006
Beaudet, Arthur L. Autism: highly heritable but not inherited. Nature Medicine. Vol. 13 No. 5, p. 534-6, 2007
Maimburg, Rikke D. and M. Vaeth. Do children born after assisted conception have less risk of developing infantile autism? European Society of Human Reproduction and Embryology. p.1-3, 2007
Cantor, RM. et al. Paternal age and autism are associated in a family-based sample. Molecular Psychiatry. Vol. 12. p. 419-423, 2007
Nagarajan, R.P. et al. Reduced MeCP2 expression is frequent in autism frontal cortex and correlates with aberrant MECP2 promoter methylation. Epigenetics. Vol. 1, No. 4, p. 172-182, 2006.
Hypertextbook, http://hypertextbook.com/facts/1998/StevenChen.shtml
