Can Science Reveal an Underlying Cause of Adhd?Essay Preview: Can Science Reveal an Underlying Cause of Adhd?Report this essayCan Science Reveal an Underlying Cause?Scientific research regarding Attention-deficit Hyperactivity Disorder (ADHD) identifies important genetic predispositions, environmental factors, and social behaviors involved with the diagnosis of this psychiatric disorder. The complexity of the possible developmental pathways associated with ADHD has created enormous challenges for scientific research. Today, scientists are collaborating their research efforts to understand the mechanical, physical and neurobiological abnormalities underlying ADHD.
ADHD is characterized by three primary symptoms: impulsiveness, hyperactivity, and inattention, and it is one of the most common childhood psychiatric disorders . Currently, the DSM-IV categorizes 3 sub-types of ADHD: (1) primarily inattentive, (2) primarily impulsive and hyperactive and (3) a combination of the first two. The criteria contain over 18 potential symptoms categorized by the different subtypes. (Ilina 2008) It affects about 3-7% of children globally with symptoms starting before the age of seven years old. As of 2006, 4.5 million Americans ages 5-17 years old have been diagnosed with ADHD. (Bloom 2007) A study conducted by the National Institute of Mental Health Association revealed the potential associations ADHD has with other psychiatric disorders. The cluster of behavioral symptoms that are relevant in ADHD are highly correlated with other psychiatric disorders such as oppositional defiant disorder (40%), anxiety disorder (34%), conduct disorder (14%), tic disorder (11%) and mood disorders (4%). (Ilina 2008)
Today, there is no cure for ADHD but available treatment focuses on reducing symptoms caused by the neurological imbalances. The most common treatment is methylphenidate, a psychostimulant, which provides therapeutic effects by blocking the reuptake of dopamine into nerve terminals and stimulating release of dopamine from dopamine nerve terminals. (Spencer 2007) The use of methylphenidates has been implicated in many research studies to provide further explanation of the neurobiochemical mechanisms implicated in ADHD.
The global increase in ADHD diagnoses has led to a national debate concerning the efficacy of treatment, especially in children. Currently, there are many controversies involving the validity of the diagnosis of ADHD. One of the problems that exist is there is no known etiology that addresses all underlying issues in ADHD. There are many concerns that the DSM-IV criteria are too subjective in nature, and there is no clinical test to confirm the diagnosis. This has sparked a national debate especially with the increase of people being diagnosed and treated with methylphenidates. (Wikipedia 2009) Today, scientific evidence has revealed some potential side effects in long-term therapy. Long-term effects include paranoia, anxiety, euphoria, confusion, increased aggression and irritability. Abuse of these drugs can lead to drug dependence, withdrawal effects and even psychosis. Ultimately, more research must be done to demonstrate the long-term effects of methylphenidates on the developing brain and the possibility of mental health issues arising later in life. (Durston 2008)
The key factor of ADHD is the abnormal interaction between monoamine transmitters within the brain. ADHD is a neurologically complex developmental disorder primarily affecting the dopaminergic and noradrenergic pathways within the brain. The dopaminergic pathways transmit the neurotransmitter dopamine from one area of the brain to another. Evidence suggests that ADHD plays a significant role in the disruption of the corticostriatal circuits, which are responsible for transmission of dopamine from the Ventral tegmental area to the prefrontal cortex and from the substantia nigra to the corpus striatum. The dysfunction in the dopamine neurotransmitter system interferes with important pathways that aid in attention and motivation. Also, there is evidence that disruption of dopaminergic pathway gives rise to a lack of tolerance of delayed reward and contributes to impulsiveness related to ADHD. (Spencer 2009) The noradrenergic neurons originate in the locus coeruleus located in the pons. The locus coeruleus contains many projectile pathways When these neurons are activated they play a large role in alertness, arousal and influence the reward system. (Durston 2008)
Genetic studies have played a leading role in clarifying the biological basis of this disorder. Many studies have been performed that provide evidence of a familial linkage specifically in twin studies. Twin studies show that ADHD is highly heritable and genes account for 75% of the disorders variability in the population. (Illina 2008) Given the strong evidence from studies performed, scientists are continuing to identify genes that increase susceptibility to ADHD. Specific genes in ADHD research have been identified, and their risk factors in relation to ADHD have been determined. Two genes are the TACR1 receptor gene and the dopamine D4 receptor gene, also known as the 7-repeat variant. The DDR4 gene, 7-repeat variant, accounts for 30% of the genetic risk for ADHD, making it one of the strongest candidate genes implicated in this disorder.(Grady 2005) The TACR1 gene is expressed by cholinergic neurons in the dorsal striatum and the PFC. Recently, the discovery
is that TACR1 receptors have been associated with more and more of the symptoms of this disorder, which include a significantly increased risk factor for AD and related chronic inflammation. Based on a review of 16 known polymorphisms, these neuropathological polymorphisms have been identified as the TACR1rD5 gene(Grady 2004). (Grady 2005) This gene is significantly associated with ADHD, which correlates with elevated risks of the disorder. However, the etiology of TACR1rD5 is a complex genetic phenomenon, especially in relation to individuals with ADHD. Because it can be found in association with a common genetic or phenotypic defect, the etiology of ADHD is still largely unknown, but there are a large number of novel genetic variants that would have genetic effects on the development of this disease. The TACR1rD5 gene can also play a role in promoting the development of ADHD. For example, a genetic variant that is also often associated with elevated risk of AD development has been identified, especially in connection with a genetic variant in the ABA that is commonly referred to as the hyperactivity disorder TACR2 (Lingford et al 2005). In some cases, the genetic association between ADHD and a genetic mutation can lead asthmatics to identify ADHD genetic variants that mimic or cause other disorders. In others, however, genetic variants that occur in conjunction with ADHD, such as ADHD-6 or ADHD-8 gene variants (eg, genes related to dopamine B4 synthesis) have been identified and identified.(Lingford et al 2005) Research into genetic predisposition to ADHD often begins from a small sample of children over 10 years of age, as the age for which we can look for potential genetic variants can quickly increase. Research is carried out by the National Institute of Mental Health, which is an independent agency responsible for developing, improving and supporting research programs that address the health, safety and well being of children in the United States. As the National Institutes of Health has long supported research that promotes and supports the health and well being of children, we have sought to increase public awareness of what is known about genetic and developmental factors related to ADHD in children, but not how these children are actually affected. For instance, the National Institutes of Health, in its publication on ADHD, stated (as has been reported extensively by many other sources) that the development and prevalence of psychiatric disorders and disorders associated with ADHD are increasing throughout the world. Because this is a major global concern for the United States and the rest of the world,[1] it has been imperative that we identify and study the genetic basis of this disease. At the highest levels, this is a research issue involving many scientists, academics, and clinicians. However, a very small number of these researchers remain committed to conducting a major study on the genetic etiology and phenotypes of ADHD in children. Research on the genetics of ADHD in children is primarily focused on children born to parents with ADHD (M.M.) and those over the age of 18. Furthermore, many of these children are very similar and are very likely to meet the genetic criteria for ADHD. The genetic background of ADHD, as it relates to a biological process such as hyperactivity disorder and hyperactivity
adolescence has been known through several generations, including for all people since the first human beings were first born. This research has led to the understanding of ADHD as characterized by a genetic component that is usually present in the first year of life, and for those children who are found at risk in the first year of life, in that there are many genetic variants that increase the risk of ADHD. The most common variant is the ADHD-CAGD1 gene (called The DAGD1a gene), which causes an increase in the risk for ADHD when used in conjunction with a stimulant drug. The genetic