ADHD IS NOT A MYTH.....

 

Whether you are an adult, adolescent or child, ADHD is NOT a myth - it impacts self-esteem, relationships, work-life, and school-life.

The Centre for ADHD is dedicated to providing support services designed to assist you in living well with ADHD.

We offer a full range of services including:

· ADHD Assessments

· Skill Development Groups

· Coaching

· Lifestyle Strategies

· Mindfulness

· Goal Setting

· Psychoeducation

· Healthy Communication

· Interpersonal Effectiveness

· Relationship Building

Many people have heard of ADHD.

It may make you think of kids who have trouble paying attention or who are hyperactive or impulsive. Adults can have ADHD, too. About 4% to 5% of U.S. adults have it. But few adults get diagnosed or treated for it.

Who gets adult ADHD? Every adult who has ADHD had it as a child. Some may have been diagnosed and known it. But some may have not been diagnosed when they were young and only find out later in life.

While some kids with ADHD outgrow it, about 60% to 80% of children who are diagnosed with ADHD will still have symptoms when they are teens or adults, although their symptoms may become less obvious over time. Adult ADHD appears to affect men and women equally.

ADHD Runs in Families and is Highly Heritable

The first hint that genetic factors may play a role in ADHD came from research findings indicating that ADHD runs in families. For instance, compared to their non-ADHD peers, students with ADHD are two to eight times more likely to have at least one sibling with ADHD and to have a parent with ADHD, although the symptoms of ADHD may never have been identified or formally diagnosed in the family members.

Family studies cannot separate the effect of genes from possible environmental factors. To directly estimate the heritability of ADHD, twins need to be studied. Monozygotic ("identical") twins share 100% of their genes, whereas dizygotic ("fraternal") twins, like other siblings, share about 50% of their genes on average. Researchers determine the extent to which identical twins are concordant for ADHD (that is, the chance that if one twin has ADHD, the other will as well) and compare this to the rate in fraternal twins. From this information, researchers can then compute the heritability of ADHD, or the degree to which variability in ADHD in the population can be accounted for by genes. The mean heritability estimate for ADHD across about 20 twin studies is roughly 80%, indicating that ADHD is highly heritable — almost as heritable as height!

From the school perspective, these findings mean that if a student with ADHD has siblings, one or more of the other siblings are likely to also have ADHD. But siblings with ADHD may show very different profile of ADHD symptoms and also may have different types of problems at school (for example, one sibling may have concurrent reading disabilities, whereas the other sibling may have additional problems with aggression or non-compliance). Thus, what worked for teaching and managing classroom behaviour for one of the siblings may not be effective with the other; a functional assessment of each student's strengths and difficulties is always required. It is also possible that one of the parents of the student with ADHD may have ADHD themselves. ADHD in adulthood poses additional challenges for parenting, particularly if both parent and child have ADHD.

Genetic Factors in ADHD

The high heritability of ADHD has stimulated investigations into the molecular genetic basis of ADHD. Converging evidence from pharmacological, neuroimaging, and animal research has focused the molecular genetic research primarily on genes involved in specific neurotransmitter systems, particularly the dopamine system. At the time this website was created, there have been only a few genome-wide scans and no specific chromosomal region has been implicated unequivocally. Nonetheless, considerable progress has been made and several genes have been identified that increase the susceptibility to ADHD, including the dopamine D4 receptor gene (DRD4), the dopamine transporter gene (DAT1), and the dopamine D5 receptor (DRD5), as well as genes associated with the other neurotransmitters (noradrenaline, serotonin), and synaptosomal proteins, such as the SNAP-25 protein. However, these genes confer only a small additional risk of ADHD on their own and the general belief is that this complex disorder involves multiple genes of small to moderate effect. Researchers are now beginning to investigate how such genes work together and how they interact with environmental factors to influence behaviour. Researchers are also trying to identify patterns of genetic variation that may make it possible to develop individually tailored pharmacological treatments for this disorder.

Environmental Factors contribute to ADHD

Twin studies indicate not only that ADHD is highly heritable, but also that 10% to 25% of the variance in the ADHD phenotype is accounted for mostly by non-shared environmental factors, and that shared environmental factors play only a small role in increasing the risk for ADHD.

Pregnancy, labour and delivery, and neonatal complications are associated with an increased risk for ADHD in childhood. Problems in the neonatal period, such as the need for an incubator, oxygen therapy, or surgery, are more common in children with ADHD than in their siblings, suggesting that neonatal complications may be a non-shared environmental risk factor. Other perinatal problems (that is, problems relating to the period around childbirth, especially the five months before, during, and one month after birth), such as prenatal exposure to nicotine or alcohol, prematurity, and low birth weight, are also associated with increased risk for ADHD and academic difficulties. For example, children of mothers who smoke during pregnancy are more likely to be rated by parents and teachers as exhibiting symptoms of inattention (or ADHD) and to exhibit lower academic achievement and poorer visuo-spatial reasoning. Also, children with ADHD are 2.5 times more likely to have been exposed to alcohol in utero and 2 times more likely to be exposed prenatally to cigarette smoke than non-ADHD control subjects. Moreover, maternal smoking during pregnancy is associated with lower levels of specific neurotransmitters (such as dopamine) in the fetus and elevated risk for subsequent nicotine dependence in adulthood in the offspring. However, the link between maternal smoking in pregnancy and increased risk for ADHD in the offspring may be shared family risks that interact to some degree with genetics.

Some toxic chemicals in the environment are known to interfere with the same aspects of behaviour and learning that are atypical in ADHD, and so are also thought to play a causal role. Lead is the best-studied example of an environmental contaminant that interferes with learning. Exposure to lead causes reductions in IQ and has also been linked to reading and learning disabilities, disruptive behaviour in the classroom, and reduced ability to pay attention. Lead exposure is also associated with increased risk for antisocial and delinquent behaviour in childhood and is a predictor of adult criminality.

Other toxic chemicals that have been shown to interfere with children's learning are the polychlorinated biphenyls (PCBs), chemical insulators that were widely used by industry until their ban in the U.S. in 1976 and that persist in the environment and in human tissue. Children are exposed to PCBs through breast milk and by eating fish and other fatty foods that contain high concentrations of PCBs. Children can also be exposed in utero, as PCBs move across the placenta. Exposure to high levels of PCBs has been shown to interfere with many aspects of cognitive development, including lower full-scale and verbal IQ scores as well as significant attention and memory deficits.

 

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