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ADHD, or Attention Deficit Hyperactivity Disorder, is a widespread childhood disorder that has received a great deal of focus in recent years. According to estimates, nearly 10 percent of all children and 4 percent of adults are affected with ADHD.
Symptoms of this frequently-occurring disorder include hyperactivity, distractibility, and impulsivity; these symptoms often lead to difficulties performing in work or school, and they may also increase the risk of accidents. Individuals with ADHD also have an increased likelihood of experiencing emotional disorders such as depression and anxiety.
Typically, adults with ADHD are unaware that they have this disorder – they often just feel that it’s impossible to get organized, to stick to a job, to keep an appointment. The everyday tasks of getting up, getting dressed and ready for the day’s work, getting to work on time, and being productive on the job can be major challenges for the ADHD adult. ADHD alternative treatment consists of treating the underlying cause of the disorder, not just masking the symptoms with medication.
The precise causes of ADHD are not yet fully understood, but it is clear that the disorder is influenced by the interaction of environmental, genetic, and neurological factors; the structure of the brain may play a role, as well. Many specialists in ADHD also believe that nutritional issues may have an impact on the disease.
There is some evidence that people with ADHD do not produce adequate quantities of certain neurotransmitters, among them dopamine, norepinephrine, and serotonin. Some experts theorize that such deficiencies lead to self-stimulatory behaviors that can increase brain levels of these chemicals (Comings DE et al 2000; Mitsis EM et al 2000; Sunohara GA et al 2000).
Epinephrine activation of receptors on the cranial vagus nerve increases the release of central norepinephrine and has been shown to enhance memory formation. Patients with ADHD have been shown to have a reduced urinary epinephrine level. Contrary findings are seen in patients with anxiety or PTSD. Given the high incidence of anxiety within ADHD patients, as well as the increased risk of accident and injury, testing of epinephrine in ADHD patients should consider these other factors in order to have a better understanding of the role of epinephrine in ADHD.
ADHD is believed to be in part the result of a reduced or hypodopaminergic state. In conjunction with this assumption are the needs for stronger and less delayed behavioral reinforcement. Dopamine is involved in the reward cascade, and the increased reinforcement threshold may be a manifestation of the hypodopaminergic state. Children with ADHD have displayed normal task performance under conditions of high incentive, but deficient performance under conditions of low incentive. Methylphenidate is believed to be beneficial in ADHD in part due to its ability to enhance dopamine signaling, and therefore may enhance a deficient reward system in ADHD patients.
The development of the dopamine system prior to and during early adolescence is quite rapid, while the development of the serotonin system during this same time remains steady. A relative deficit in dopamine maturity would be concordant with an increased impulsivity and increased reward threshold seen in ADHD.
A delayed rate of brain development in ADHD is also supported by studies that find patients have an increased level of delta and theta brain wave activity compared to controls. Delta and theta brain wave activity normally decreases until adulthood. As such, increased delta and theta brain wave activity can be an indicator of slowed brain maturity. Differences in the rate of serotonin and dopamine system development also may explain why significant numbers of children outgrow their ADHD symptoms.
Norepinephrine is an excitatory neurotransmitter that is important for attention and focus. Norepinephrine is synthesized from dopamine by means of the enzyme dopamine beta-hydroxylase, with oxygen, copper, and vitamin C as co-factors. Dopamine is synthesized in the cytoplasm, but norepinephrine is synthesized in the neurotransmitter storage vesicles.; Cells that use norepinephrine for the formation of epinephrine use SAMe as a methyl group donor. Levels of epinephrine in the CNS are only about 10% of the levels of norepinephrine.
The noradrenergic system is most active when an individual is awake, which is important for focused attention. Elevated norepinephrine activity seems to be a contributor to anxiousness. Also, brain norepinephrine turnover is increased in conditions of stress. Interestingly, benzodiazepines, the primary anxiolytic drugs, decrease firing of norepinephrine neurons.
PEA (phenylethylamine) is an excitatory neurotransmitter that tends to be lower in patients with ADHD. Studies that tested urine levels of PEA in subjects with ADHD during treatment with stimulants (methylphenidate or dextroamphetamine), found that the levels of PEA were increased. Additionally, studies report that the efficacy of the treatment correlated positively with the degree to which urinary PEA increased.
Many of the effects of serotonin occur due to its ability to modify the actions of other neurotransmitters. Specifically, serotonin regulates dopamine release. This is evident in the observation that antagonists of either the 5-HT2a or the 5-HT2c serotonin receptor will stimulate dopamine outflow while agonists inhibit dopamine outflow. Similarly, dopamine has a regulatory effect on serotonin and neonatal damage to the dopamine system has been shown to cause large increases in serotonin.
Aspects of the interaction between serotonin and dopamine are believed to affect attention. Evidence of this interaction is present in the observation that reduced serotonin synthesis impairs the positive effects of methylphenidate on learning. Meaning some aspects of methylphenidate’s therapeutic effects require serotonin. Serotonin levels are significantly affected by stress and coping abilities combined with other environmental factors and the person’s genetic make-up to determine serotonin activity.
There may also be some structural and functional abnormalities in the brain itself in children who have ADHD (Pliszka SR 2002; Mercugliano M 1999). Evidence suggests that there may be fewer connections between nerve cells. This would further impair neural communication already impeded by decreased neurotransmitter levels (Barkley R 1997). Evidence from functional studies in patients with ADHD demonstrates decreased blood flow to those areas of the brain in which “executive function,” including impulse control, is based (Paule MG et al 2000). There may also be a deficit in the amount of myelin (insulating material) produced by brain cells in children with ADHD (Overmeyer S et al 2001).
Some prenatal factors that increase the risk of developing ADHD have been identified. These include complications during pregnancy that limit oxygen supply to the brain such as toxemia and eclampsia. Other factors during pregnancy that have an impact on normal prenatal development and increase the risk of a child developing ADHD include smoking and fetal alcohol syndrome.
Other factors, such as stress, significantly affect the way the brain functions. If the temperament of the individual under stress allows them to cope in a positive manner, stress can actually increase performance and health. If, however, the temperament of the individual under stress is such that the individual does not cope with the stress, the adaptive changes that allow the body to enhance its performance and stress may fail to function. This may lead to either an inability of the body to compensate or the inactivation of some neurological systems. Alternatively, neurological systems may become chronically elevated. In either case, the altered functions of these regions may underlie clinical symptoms.
Attention disorders often run in families, so there are likely to be genetic influences. Studies indicate that 25 percent of the close relatives in the families of ADHD children also have ADHD, whereas the rate is about 5 percent in the general population. Many studies of twins now show that a strong genetic influence exists in the disorder.
Researchers continue to study the genetic contribution to ADHD and to identify the genes that cause a person to be susceptible to ADHD. Since its inception in 1999, the Attention-Deficit Hyperactivity Disorder Molecular Genetics Network has served as a way for researchers to share findings regarding possible genetic influences on ADHD.
Studies have shown a possible correlation between the use of cigarettes and alcohol during pregnancy and risk for ADHD in the offspring of that pregnancy. As a precaution, it is best during pregnancy to refrain from both cigarette and alcohol use.
Another environmental agent that may be associated with a higher risk of ADHD is high levels of lead in the bodies of young preschool children. Since lead is no longer allowed in paint and is usually found only in older buildings, exposure to toxic levels is not as prevalent as it once was. Children who live in old buildings in which lead still exists in the plumbing or in lead paint that has been painted over may be at risk.
One early theory was that attention disorders were caused by brain injury. Some children who have suffered accidents leading to brain injury may show some signs of behavior similar to that of ADHD, but only a small percentage of children with ADHD have been found to have suffered a traumatic brain injury.
As previously mentioned, ADHD is most likely caused by multiple factors, including nutritional issues. Children and adults with ADHD may have specific nutrient deficiencies that aggravate their condition.
Dopamine Supplements contain the building blocks needed for the brain to produce more Dopamine.
Omega-3 fatty acids are essential components of brain cell membranes, including those of neurotransmitter receptors. Omega-3 fatty acids also alter signal transduction and electrical activity in brain cells and control the synthesis of chemicals such as eicosanoids and cytokines, which may have a direct effect on mood and behavior. Evidence supporting the role of fatty acid imbalances in the pathology of ADD/ADHD:
Research consistently finds people with ADD/ADHD have lower levels of essential fatty acids than controls. A large proportion of people with ADD/ADHD display essential fatty acid deficiency symptoms (e.g. excessive thirst, frequent urination, vision impairment, dry skin and hair, learning difficulties.)
Magnesium and vitamin B6. Combining magnesium and vitamin B6 has shown promise for reducing symptoms of ADHD. Vitamin B6 has many functions in the body, including assisting in the synthesis of neurotransmitters and forming myelin, which protects nerves. Magnesium is also very important; it is involved in more than 300 metabolic reactions. At least three studies have demonstrated that the combination of magnesium and vitamin B6 improved behavior, decreased anxiety and aggression, and improved mobility among children with ADHD (Nogovitsina OR et al 2006a,b; Nogovitsina OR et al 2005; Mousain-Bosc M et al 2004).
Zinc. Zinc is a cofactor for production of neurotransmitters, fatty acids, prostaglandins, and melatonin, and it indirectly affects the metabolism of dopamine and fatty acids. Numerous studies have shown that children with ADHD are often deficient in zinc.
Acetyl-L-carnitine. This superior form of L-carnitine, which is responsible for transporting fatty acids into the mitochondria, has been associated with a host of positive health benefits, including reducing impulsivity. In an animal model of ADHD, acetyl-L-carnitine was shown to reduce the impulsivity index (Adriani W et al 2004).
Melatonin. Melatonin is a hormone secreted at night by the pineal gland. It participates in multiple body processes, including regulation of the sleep/wake cycle. Because many children and adults who have ADHD also have sleep problems, melatonin can be an important part of an integrative therapy. By some estimates, up to 25 percent of children with ADHD also have sleep disorders. Unfortunately, however, conventional therapy treats the hyperactivity portion of the disease but neglects the sleep disorder (Betancourt-Fursow de Jimenez YM et al 2006). In one study of 27 children with ADHD and insomnia, 5 milligrams (mg) of melatonin, combined with sleep therapy, helped reduce insomnia (Weiss MD et al 2006).
Dehydroepiandrosterone (DHEA). DHEA is an important neuroactive steroid hormone that may be involved in ADHD, although researchers are still trying to understand the relationship. ADHD is associated with low blood levels of DHEA, its principal precursor pregnenolone, and its principal metabolite dehydroepiandrosterone-sulfate (DHEA-S). Higher blood levels of these neurosteroids are associated with fewer symptoms (Strous RD et al 2001). Furthermore, a study of adolescent boys with ADHD showed that DHEA levels rise after a 3-month course of methylphenidate treatment, which implies that DHEA somehow plays a role in the drug’s effectiveness (Maayan R et al 2003).
Ginkgo biloba and ginseng. A combination of these two herbs has been studied for its ability to improve symptoms among patients with ADHD. In a study of 36 children ranging in age from 3 to 17 years old, a combination of Ginkgo biloba and American ginseng was administered twice a day on an empty stomach for 4 weeks. At the end of the study, more than 70 percent of patients had experienced improvement on a widely used measure of ADHD symptoms (Lyon MR et al 2001).
Dietary interventions (as contrasted with dietary supplements) are based on the concept of elimination, that one or more foods are eliminated from one’s diet.
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